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Ozdemir, Tugba, Pu Zhang, Changliang Fu, and Cheng Dong. "Fibrin serves as a divalent ligand that regulates neutrophil-mediated melanoma cells adhesion to endothelium under shear conditions." American Journal of Physiology-Cell Physiology 302, no. 8 (April 15, 2012): C1189—C1201. http://dx.doi.org/10.1152/ajpcell.00346.2011.
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Elevated soluble fibrin (sFn) levels are characteristic of melanoma hematogeneous dissemination, where tumor cells interact intimately with host cells. Melanoma adhesion to the blood vessel wall is promoted by immune cell arrests and tumor-derived thrombin, a serine protease that converts soluble fibrinogen (sFg) into sFn. However, the molecular requirement for sFn-mediated melanoma-polymorphonuclear neutrophils (PMNs) and melanoma-endothelial interactions under physiological flow conditions remain elusive. To understand this process, we studied the relative binding capacities of sFg and sFn receptors e.g., αvβ3integrin and intercellular adhesion molecule-1 (ICAM-1) expressed on melanoma cells, ICAM-1 on endothelial cells (EC), and CD11b/CD18 (Mac-1) on PMNs. Using a parallel-plate flow chamber, highly metastatic melanoma cells (1205Lu and A375M) and human PMNs were perfused over an EC monolayer expressing ICAM-1 in the presence of sFg or sFn. It was found that both the frequency and lifetime of direct melanoma adhesion or PMN-facilitated melanoma adhesion to the EC in a shear flow were increased by the presence of sFn in a concentration-dependent manner. In addition, sFn fragment D and plasmin-treated sFn failed to increase melanoma adhesion, implying that sFn-bridged cell adhesion requires dimer-mediated receptor-receptor cross-linking. Finally, analysis of the respective kinetics of sFn binding to Mac-1, ICAM-1, and αvβ3by single bond cell tethering assays suggested that ICAM-1 and αvβ3are responsible for initial capture and firm adhesion of melanoma cells. These results provide evidence that sFn enhances melanoma adhesion directly to ICAM-1 on the EC, while prolonged shear-resistant melanoma adhesion requires interactions with PMNs.
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Bauschlicher, Charles W., and Alessandra Ricca. "Accurate Heats of Formation for SFn, SFn+, and SFn-forn= 1−6." Journal of Physical Chemistry A 102, no. 24 (June 1998): 4722–27. http://dx.doi.org/10.1021/jp981084p.
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Son, Eun Suk, Xiang Fei, Jin-Ha Yoon, Seung-Yong Seo, Han-Joo Maeng, Sung Hwan Jeong, and Yu Chul Kim. "Comparison of Pharmacokinetics and Anti-Pulmonary Fibrosis-Related Effects of Sulforaphane and Sulforaphane N-acetylcysteine." Pharmaceutics 13, no. 7 (June 25, 2021): 958. http://dx.doi.org/10.3390/pharmaceutics13070958.
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Sulforaphane (SFN), belonging to the isothiocyanate family, has received attention owing to its beneficial activities, including chemopreventive and antifibrotic effects. As sulforaphane N-acetylcysteine (SFN-NAC), a major sulforaphane metabolite, has presented similar pharmacological activities to those of SFN, it is crucial to simultaneously analyze the pharmacokinetics and activities of SFN and SFN-NAC, to comprehensively elucidate the efficacy of SFN-containing products. Accordingly, the anti-pulmonary fibrotic effects of SFN and SFN-NAC were assessed, with simultaneous evaluation of permeability, metabolic stability, and in vivo pharmacokinetics. Both SFN and SFN-NAC decreased the levels of transforming growth factor-β1-induced fibronectin, alpha-smooth muscle actin, and collagen, which are major mediators of fibrosis, in MRC-5 fibroblast cells. Regarding pharmacokinetics, SFN and SFN-NAC were metabolically unstable, especially in the plasma. SFN-NAC degraded considerably faster than SFN in plasma, with SFN being formed from SFN-NAC. In rats, SFN and SFN-NAC showed a similar clearance when administered intravenously; however, SFN showed markedly superior absorption when administered orally. Although the plasma SFN-NAC concentration was low owing to poor absorption following oral administration, SFN-NAC was converted to SFN in vivo, as in plasma. Collectively, these data suggest that SFN-NAC could benefit a prodrug formulation strategy, possibly avoiding the gastrointestinal side effects of SFN, and with improved SFN-NAC absorption.
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Mans, Jaylen C., and Xiaowei Dong. "The Development of Lipid-Based Sorafenib Granules to Enhance the Oral Absorption of Sorafenib." Pharmaceutics 15, no. 12 (November 28, 2023): 2691. http://dx.doi.org/10.3390/pharmaceutics15122691.
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Sorafenib (SFN) is an anticancer multi-kinase inhibitor with great therapeutic potential. However, SFN has low aqueous solubility, which limits its oral absorption. Lipids and surfactants have the potential to improve the solubility of water-insoluble drugs. The aim of this study is thus to develop novel lipid-based SFN granules that can improve the oral absorption of SFN. SFN powder was coated with a stable binary lipid mixture and then absorbed on Aeroperl 300 to form dry SFN granules with 10% drug loading. SFN granules were stable at room temperature for at least three months. Compared to SFN powder, SFN granules significantly increased SFN release in simulated gastric fluid and simulated intestinal fluid with pancreatin. Pharmacokinetics and tissue distribution of SFN granules and SFN powder were measured following oral administration to Sprague Dawley rats. SFN granules significantly increased SFN absorption compared to SFN powder. Overall, the lipid-based SFN granules provide a promising approach to enhancing the oral absorption of SFN.
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He, Lixia, Hanmin Jiang, Yaotong Li, Xu Zhang, Wenting Sun, Ce Liu, Zekai Zhao, Chengrong Yun, Hui Li, and Chunguo Wang. "Sulforaphane-Enriched Extracts from Broccoli Exhibit Antimicrobial Activity against Plant Pathogens, Promising a Natural Antimicrobial Agent for Crop Protection." Biomolecules 14, no. 3 (March 14, 2024): 352. http://dx.doi.org/10.3390/biom14030352.
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Sulforaphane (SFN) is one of the hydrolysates of glucosinolates (GSLs), primarily derived from Brassica vegetables like broccoli. In clinical therapy, SFN has been proven to display antimicrobial, anticancer, antioxidant, and anti-inflammatory properties. However, the antimicrobial effects and mechanism of SFN against plant pathogens need to be further elucidated, which limits its application in agriculture. In this study, the genetic factors involved in SFN biosynthesis in 33 B. oleracea varieties were explored. The finding showed that besides the genetic background of different B. oleracea varieties, myrosinase and ESP genes play important roles in affecting SFN content. Subsequently, the molecular identification cards of these 33 B. oleracea varieties were constructed to rapidly assess their SFN biosynthetic ability. Furthermore, an optimized protocol for SFN extraction using low-cost broccoli curds was established, yielding SFN-enriched extracts (SFN-ee) containing up to 628.44 μg/g DW of SFN. The antimicrobial activity assay confirmed that SFN-ee obtained here remarkably inhibit the proliferation of nine tested microorganisms including four plant pathogens by destroying their membrane integrity. Additionally, the data demonstrated that exogenous application of SFN-ee could also induce ROS accumulation in broccoli leaves. These results indicated that SFN-ee should play a dual role in defense against plant pathogens by directly killing pathogenic cells and activating the ROS signaling pathway. These findings provide new evidence for the antimicrobial effect and mechanism of SFN against plant pathogens, and suggest that SFN-ee can be used as a natural plant antimicrobial agent for crop protection and food preservation.
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Cheung, Y. S., Y. J. Chen, C. Y. Ng, See-Wing Chiu, and Wai-Kee Li. "Combining Theory with Experiment: Assessment of the Thermochemistry of SFn, SFn+, and SFn-, n = 1-6." Journal of the American Chemical Society 117, no. 38 (September 1995): 9725–33. http://dx.doi.org/10.1021/ja00143a016.
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Wang, Shiyu, Yanan Wang, Xiangnan Liu, Yongbin Yang, Sufang Wu, and Yuan Liu. "SFN Enhanced the Radiosensitivity of Cervical Cancer Cells via Activating LATS2 and Blocking Rad51/MDC1 Recruitment to DNA Damage Site." Cancers 14, no. 8 (April 8, 2022): 1872. http://dx.doi.org/10.3390/cancers14081872.
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Background: Sulforaphane (SFN) is one kind of phytochemical anticancer drug. It inhibits cancer cell proliferation and promotes cell apoptosis while the mechanism behind is still uncertain. We aimed to explore its downstream target and the radiotherapy sensitization mechanism in cervical cancer. Methods: We treated established cervical cancer cells line (SiHa, HeLa, C33A) with SFN followed by irradiation, and explored its survival, apoptosis, and DNA damage repair in vitro and validated the radiosensitivity of SFN treatment in vivo. We conducted mRNA sequencing to identify differentially expressed mRNAs after SFN treatment. We further investigated SFN downstream target and its involvement in DNA damage repair under irradiation. Results: We found that SFN inhibited the survival of cervical cancer cells under radiotherapy treatment in vitro and prolonged the survival period after radiotherapy in the mouse tumorigenic model. SFN increased the protein expression of LATS2 and promoted apoptosis of cervical cancer cells. Overexpressed LATS2 decreased the cellular survival rate of cervical cancer cells. Additionally, SFN treatment and LATS2 overexpression prevented MDC1 and Rad51 from accumulating in the nucleus in cervical cancer cells after being exposed to ionized radiation. LATS2 loss intervened with SFN-alleviated RAD51 and MDC1 nucleus accumulation and resumed the repairment of DNA damage. Conclusion: We identified SFN as cervical cancer cells radiotherapy sensitizer and LATS2 served as a downstream target of SFN treatment. SFN treatment resulted in the inhibition of the homologous recombination (HR) pathway, and LATS2 has an indispensable contribution to this SFN-facilitated radiotherapy sensitization.
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Martins, Tânia, Tiago Ferreira, Bruno Colaço, Beatriz Medeiros-Fonseca, Maria de Lurdes Pinto, Ana Novo Barros, Carlos Venâncio, et al. "Absorption and Excretion of Glucosinolates and Isothiocyanates after Ingestion of Broccoli (Brassica oleracea L. var italica) Leaf Flour in Mice: A Preliminary Study." Nutraceuticals 3, no. 4 (November 2, 2023): 540–55. http://dx.doi.org/10.3390/nutraceuticals3040039.
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During the harvesting of the broccoli plant, the leaves are discarded, being considered a by-product that may be up to 47% of total broccoli biomass, representing a large amount of wasted material. The use of broccoli leaves is of great interest in the sense that this wasted material is rich in health promoter compounds, such as isothiocyanates. In this study, C57BL/6J mice ingested 790 mg/kg broccoli leaf flour, and the presence of glucosinolates and isothiocyanates in the plasma, liver, kidney, adipose tissue, faeces and urine was analysed at 1, 2, 4, 8, 12 and 24 h post-ingestion. In plasma, only glucoerucin (GE), glucobrassicin (GB), sulforaphane (SFN) and indol-3-carbinol (I3C) were detected, and all four compounds peaked between 4 and 8 h after ingestion. The compounds SFN, SFN-glutathione (SFN-GSH), SFN–cysteine (SFN-CYS) and SFN-N-acetyl-cysteine (SFN-NAC) were excreted in faeces at high levels, while glucoraphanin (GR), the precursor of SFN, was not detected in any biological samples other than urine. In the liver, the compounds GE, SFN-CYS, SFN-NAC and I3C were detected, while in the kidney, only GE, GB and SFN-GSH were present. None of the glucosinolates and isothiocyanates analysed were detected in fat tissue. These results demonstrate that glucosinolates and their derivatives were absorbed into the bloodstream and were bioavailable after ingestion of powdered broccoli leaves.
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Mehdi, Bagheri, Fazli Mozghan, Arzaghi Sogand, and Ahmadiankia Naghmeh. "Sulforaphane Modulates Metastasis Related Gene Expression and Cytokine Secretion in MDA-MB-231 Breast Cancer Cells." Current Topics in Nutraceutical Research 17, no. 3 (January 18, 2019): 260–65. http://dx.doi.org/10.37290/ctnr2641-452x.17:260-265.
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Sulforaphane (SFN) a chemopreventive isothiocyanate found in cruciferous vegetables, exhibits antimetastatic properties. To address the possible molecular mechanisms underlying the antimetastatic activity of SFN we assessed the expression of some chemotactic factors, adhesion molecules, and key regulators of metastasis. For this purpose, MDA-MB-231 cells were treated with different concentrations of SFN. After 72 h, the inhibitory effects of SFN on the production of the cytokines and also expression of metastatic related genes were examined by enzyme-linked immunosorbent assay and, real-time PCR, respectively. Our results revealed that, SFN significantly decreased the secretion of TGFβ1, MCP1, and MMP9, while the level of IL8 was decreased only at high concentrations of SFN. Moreover, our findings showed that, SFN significantly downregulated the expression of VCAM1, fibronectin, and VEGF while, there was no significant difference in gene expression of ICAM1 after 72 h. SFN treatment. According to obtained results, SFN can be considered as a potential adjuvant therapeutic agent by targeting key regulators of breast cancer metastasis.
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Cui, Wenpeng, Yang Bai, Xiao Miao, Ping Luo, Qiang Chen, Yi Tan, Madhavi J. Rane, Lining Miao, and Lu Cai. "Prevention of Diabetic Nephropathy by Sulforaphane: Possible Role of Nrf2 Upregulation and Activation." Oxidative Medicine and Cellular Longevity 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/821936.
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The present study was to investigate whether sulforaphane (SFN) can prevent diabetic nephropathy in type 1 diabetic mouse model induced by multiple low-dose streptozotocin. Diabetic and age-matched control mice were given SFN at 0.5 mg/kg body weight daily for 3 months. At the end of 3-month SFN treatment, the diabetic nephropathy, shown by renal inflammation, oxidative damage, fibrosis, and dysfunction, was significantly prevented along with an elevation of renal Nrf2 expression and transcription in diabetes/SFN group compared with diabetic group. However, this renal prevention by SFN was not seen when the 3-month SFN-treated diabetic mice were aged for additional 3 months without further SFN treatment. Nrf2-mediated renal protective effects in diabetes were evaluated in human renal tubular HK11 cells transfected with control and Nrf2 siRNA and treated with 27.5 mM mannitol or high glucose plus palmitate (300 μM). Blockade of Nrf2 expression completely abolished SFN prevention of the profibrotic effect induced by high glucose plus palmitate. These results support that renal Nrf2 expression and its transcription play important roles in SFN prevention of diabetes-induced renal damage. However, the SFN preventive effect on diabetes-induced renal pathogeneses is not sustained, suggesting the requirement of continual use of SFN for its sustained effect.
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Langston-Cox, Annie, Dovile Anderson, Darren J. Creek, Kirsten Palmer, Euan M. Wallace, and Sarah A. Marshall. "Measuring Sulforaphane and Its Metabolites in Human Plasma: A High Throughput Method." Molecules 25, no. 4 (February 13, 2020): 829. http://dx.doi.org/10.3390/molecules25040829.
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(1) Background: There is increasing understanding of the potential health benefits of cruciferous vegetables. In particular sulforaphane (SFN), found in broccoli, and its metabolites sulforaphane-glutathione (SFN-GSH), sulforaphane-cysteine (SFN-Cys), sulforaphane cysteine-glycine (SFN-CG) and sulforaphane-N-acetyl-cysteine (SFN-NAC) have potent antioxidant effects that may offer therapeutic value. Clinical investigation of sulforaphane as a therapeutic antioxidant requires a sensitive and high throughput process for quantification of sulforaphane and metabolites; (2) Methods: We collected plasma samples from healthy human volunteers before and for eight hours after consumption of a commercial broccoli extract supplement rich in sulforaphane. A rapid and sensitive method for quantification of sulforaphane and its metabolites in human plasma using Liquid Chromatography–Mass Spectrometry (LC–MS) has been developed; (3) Results: The LC–MS analytical method was validated at concentrations ranging between 3.9 nM and 1000 nM for SFN-GSH, SFN-CG, SFN-Cys and SFN-NAC and between 7.8 nM and 1000 nM in human plasma for SFN. The method displayed good accuracy (1.85%–14.8% bias) and reproducibility (below 9.53 %RSD) including low concentrations 3.9 nM and 7.8 nM. Four SFN metabolites quantitation was achieved using external standard calibration and in SFN quantitation, SFN-d8 internal standardization was used. The reported method can accurately quantify sulforaphane and its metabolites at low concentrations in plasma; (4) Conclusions: We have established a time- and cost-efficient method of measuring sulforaphane and its metabolites in human plasma suitable for high throughput application to clinical trials.
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Liu, Han-Jie, Lei Wang, Lin Kang, Juan Du, Sha Li, and Hui-Xian Cui. "Sulforaphane-N-Acetyl-Cysteine Induces Autophagy Through Activation of ERK1/2 in U87MG and U373MG Cells." Cellular Physiology and Biochemistry 51, no. 2 (2018): 528–42. http://dx.doi.org/10.1159/000495274.
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Background/Aims: Sulforaphane-N-acetyl-cysteine (SFN-NAC) is a sulforaphane (SFN) metabolite with a longer half-life and better blood–brain barrier permeability than those of SFN. Previous studies have found that SFN-NAC can act via ERK to destroy microtubules and inhibit cell growth in lung cancer cells. However, the underlying mechanisms are unclear, and it is unknown whether SFN-NAC can inhibit the growth of glioma. Here, we have demonstrated for the first time that SFN-NAC activates autophagy-mediated downregulation of α-tubulin expression via the ERK pathway. Methods: U87MG and U373MG cells, two widely used glioma cell lines, were utilized in this study. Apoptosis assay, western blot analysis, co-immunoprecipitation, immunostaining, and electron microscopy were used to analyze the effect of SFN-NAC on α-tubulin and its interaction with microtube-associated protein 1 light-chain 3 (LC3). Results: SFN-NAC induced cell-cycle arrest in the G2/M phase and dose-dependently induced intracellular ERK activation, autophagy, and α-tubulin downregulation. These SFN-NAC-induced effects were reversed by inhibiting the ERK pathway with its inhibitor PD98059. U87MG and U373MG cells were transfected with LC3 small interfering RNA, and the subsequent inhibition of autophagy reversed the downregulation of α-tubulin by SFN-NAC. Furthermore, co-immunoprecipitation experiments and confocal microscopy confirmed that SFN-NAC promotes the binding of LC3 with α-tubulin in the cytoplasm. Cell viability experiments demonstrate that SFN-NAC inhibits the growth of U87MG and U373MG cell colonies. Conclusion: These findings suggest that SFN-NAC is a novel potential anti-glioma agent.
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Mogal, Md Roman, Asadullah Junayed, Md Rashel Mahmod, Sagarika Adhikary Sompa, Suzana Afrin Lima, Newton Kar, TasminaTarin, Marina Khatun, Md Abu Zubair, and Md Asaduzzaman Sikder. "A Computational Approach to Justifying Stratifin as a Candidate Diagnostic and Prognostic Biomarker for Pancreatic Cancer." BioMed Research International 2022 (May 2, 2022): 1–17. http://dx.doi.org/10.1155/2022/1617989.
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Pancreatic cancer (PC) is considered a silent killer because it does not show specific symptoms at an early stage. Thus, identifying suitable biomarkers is important to avoid the burden of PC. Stratifin (SFN) encodes the 14-3-3σ protein, which is expressed in a tissue-dependent manner and plays a vital role in cell cycle regulation. Thus, SFN could be a promising therapeutic target for several types of cancer. This study was aimed at investigating, using online bioinformatics tools, whether SFN could be used as a diagnostic and prognostic biomarker in PC. SFN expression was explored by utilizing the ONCOMINE, UALCAN, GEPIA2, and GENT2 tools, which revealed that SFN expression is higher in PC than in normal tissues. The clinicopathological analysis using the ULCAN tool showed that the intensity of SFN expression is commensurate with cancer progression. GEPIA2, R2, and OncoLnc revealed a negative correlation between SFN expression and survival probability in PC patients. The ONCOMINE, UCSC Xena, and GEPIA2 tools showed that cofilin 1 is strongly coexpressed with SFN. Moreover, enrichment and network analyses of SFN were performed using the Enrichr and NetworkAnalyst platforms, respectively. Receiver operating characteristic (ROC) curves revealed that tissue-dependent expression of the SFN gene could serve as a diagnostic and prognostic biomarker. However, further wet laboratory studies are necessary to determine the relevance of SFN expression as a biomarker.
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Wen, Jing, Fan Yang, Cheng-xiang Fang, Hong-liu Chen, and Li Yang. "Sulforaphane triggers iron overload-mediated ferroptosis in gastric carcinoma cells by activating the PI3K/IRP2/DMT1 pathway." Human & Experimental Toxicology 42 (May 18, 2023): 096032712311772. http://dx.doi.org/10.1177/09603271231177295.
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Objective Increasing evidence indicates that prolonged exposure to sulforaphane (SFN) can improve malignancies. However, the role of iron in SFN-triggered death in gastric carcinoma cells and the underlying molecular mechanisms remain unclear. Thus, the current study explored the effects of SFN on iron overload-mediated ferroptosis and the PI3K/IRP2/DMT1 pathway in gastric carcinoma cells. Methods We utilized the MGC-803 cell line to assess whether SFN affected iron metabolism and whether this effect contributed to cell death. Pharmacological inhibition of iron metabolism also was performed to determine the molecular mechanism underlying SFN-triggered iron overload and the disturbance in iron metabolism. Results Our data revealed that SFN treatment altered iron homeostasis and led to iron overload in vitro. Interestingly, SFN-stimulated cell death resulted from ferroptosis, a recently identified iron-dependent form of regulated cell death. Furthermore, an iron chelator, deferiprone, ameliorated the SFN-triggered mitochondrial dysfunction and reduced the iron overload. In addition, we found that the SFN-triggered iron overload was regulated by the PI3K/IRP2/DMT1 signaling pathway. Conclusion We discovered that disturbance in iron metabolism might be involved in the SFN-triggered cell death in gastric carcinoma cells. Blockade of the PI3K/IRP2/DMT1 axis could provide a feedback effect on SFN-induced ferroptosis to protect tumor cells from growth.
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Xu, Ye, Xianghui Huang, Bingxin Huangfu, Yanzhou Hu, Jia Xu, Ruxin Gao, Kunlun Huang, and Xiaoyun He. "Sulforaphane Ameliorates Nonalcoholic Fatty Liver Disease Induced by High-Fat and High-Fructose Diet via LPS/TLR4 in the Gut–Liver Axis." Nutrients 15, no. 3 (February 1, 2023): 743. http://dx.doi.org/10.3390/nu15030743.
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The gut–liver axis has emerged as a key player in the progression of non-alcoholic fatty liver disease (NAFLD). Sulforaphane (SFN) is a bioactive compound found in cruciferous vegetables; however, it has not been reported whether SFN improves NAFLD via the gut–liver axis. C57BL/6 mice were fed a high-fat and high-fructose (HFHFr) diet, with or without SFN gavage at doses of 15 and 30 mg·kg−1 body weight for 12 weeks. The results showed that SFN reduced weight gain, hepatic inflammation, and steatosis in HFHFr mice. SFN altered the composition of gut microbes. Moreover, SFN enhanced the intestinal tight junction protein ZO-1, reduced serum LPS, and inhibited LPS/TLR4 and ERS pathways to reduce intestinal inflammation. As a result, SFN protected the intestinal integrity and declined the gut-derived LPS translocations to the liver in HFHFr diet-induced mice. SFN decreased the liver LPS levels and inhibited the LPS/TLR4 pathway activations, thus inhibiting the pro-inflammatory cytokines. Notably, Spearman correlation analysis showed that the protective effect of SFN on intestinal barrier integrity and its anti-inflammatory effect on the liver was associated with improved intestinal dysbiosis. Above all, dietary intervention with SFN attenuates NAFLD through the gut–liver axis.
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Ye, Shan-Ping, Hong-Xin Yu, Wei-Jie Lu, Jun-Fu Wang, Tai-Yuan Li, Jun Shi, and Xiao-Ye Cheng. "Stratifin Promotes Hepatocellular Carcinoma Progression by Modulating the Wnt/β-Catenin Pathway." International Journal of Genomics 2023 (August 8, 2023): 1–16. http://dx.doi.org/10.1155/2023/9731675.
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Abnormal stratifin (SFN) expression is closely related to the progression of several human cancers, but the potential roles of SFN in hepatocellular carcinoma (HCC) remain largely unknown. In this study, we found that SFN was upregulated in HCC cell lines and tissues and was positively associated with tumor size, poor differentiation, Tumor Node Metastasis (TNM) stage, and vascular invasion. In addition, high expression levels of SFN were associated with poor overall survival and disease-free survival. Biologically, downregulation of SFN suppressed tumor cell proliferation, epithelial–mesenchymal transition (EMT), invasion, and migration in vitro and tumor growth in vivo. However, overexpression of SFN promoted cell proliferation, EMT, invasion, and migration in vitro and tumor growth in vivo. Mechanistically, overexpression of SFN activated the Wnt/β-catenin pathway by promoting Glycogen synthase kinase-3 beta (GSK-3β) phosphorylation, decreasing β-catenin phosphorylation, promoting β-catenin transport into the nucleus, and enhancing the expression of c-Myc, whereas depletion of SFN inhibited the Wnt/β-catenin pathway. In addition, TOPFlash/FOPFlash reporter assays showed that overexpression or downregulation of SFN obviously increased or decreased, respectively, the activity of the Wnt/β-catenin pathway. Our results indicated that SFN plays an important role in HCC, possibly providing a prognostic factor and therapeutic target for HCC.
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Zambrano, Víctor, Rubén Bustos, Yipsy Arozarena, and Andrea Mahn. "Optimization of a Microencapsulation Process Using Oil-in-Water (O/W) Emulsion to Increase Thermal Stability of Sulforaphane." Foods 12, no. 20 (October 22, 2023): 3869. http://dx.doi.org/10.3390/foods12203869.
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Sulforaphane (SFN) is a bioactive compound widely studied for its potential applications in pharmaceutical, nutraceutical, and food industries since it offers health benefits due to its nature as a Phase 2 enzyme inducer. Its application in the food industry has been limited because SFN is unstable at high temperatures in an aqueous milieu. An option to increase SFN stability and protect it from thermal degradation is microencapsulation. The aim of this work was to optimize a microencapsulation process using oil-in-water emulsion to increase the thermal stability of SFN. The operation conditions that gave the highest entrapment efficiency were determined via experimental design and response surface methodology. Thermal degradation of microencapsulated SFN was studied at 37, 50, 60, and 70 °C. The optimum microencapsulation conditions were 8 min stirring, SFN/Gum Arabic ratio of 0.82, and surfactant/oil ratio of 1.0, resulting in an entrapment efficiency of 65%, which is the highest reported so far. The thermal stability of microencapsulated SFN was greatly enhanced compared with free SFN, with a 6-fold decrease in the degradation kinetic constant and a 41% increase in the activation energy. These results will contribute to a more efficient incorporation of SFN in various food matrices and explore new microencapsulation technologies to maximize the efficiency and stability of SFN.
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Luo, Tingting, Xiazhou Fu, Yaoli Liu, Yaoting Ji, and Zhengjun Shang. "Sulforaphane Inhibits Osteoclastogenesis via Suppression of the Autophagic Pathway." Molecules 26, no. 2 (January 12, 2021): 347. http://dx.doi.org/10.3390/molecules26020347.
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Previous studies have demonstrated that sulforaphane (SFN) is a promising agent against osteoclastic bone destruction. However, the mechanism underlying its anti-osteoclastogenic activity is still unclear. Herein, for the first time, we explored the potential role of autophagy in SFN-mediated anti-osteoclastogenesis in vitro and in vivo. We established an osteoclastogenesis model using receptor activator of nuclear factor kappa-β ligand (RANKL)-induced RAW264.7 cells and bone marrow macrophages (BMMs). Tartrate-resistant acid phosphatase (TRAP) staining showed the formation of osteoclasts. We observed autophagosomes by transmission electron microscopy (TEM). In vitro, we found that SFN inhibited osteoclastogenesis (number of osteoclasts: 22.67 ± 0.88 in the SFN (0) group vs. 20.33 ± 1.45 in the SFN (1 μM) group vs. 13.00 ± 1.00 in the SFN (2.5 μM) group vs. 6.66 ± 1.20 in the SFN (2.5 μM) group), decreased the number of autophagosomes, and suppressed the accumulation of several autophagic proteins in osteoclast precursors. The activation of autophagy by rapamycin (RAP) almost reversed the SFN-elicited anti-osteoclastogenesis (number of osteoclasts: 22.67 ± 0.88 in the control group vs. 13.00 ± 1.00 in the SFN group vs. 17.33 ± 0.33 in the SFN+RAP group). Furthermore, Western blot (WB) analysis revealed that SFN inhibited the phosphorylation of c-Jun N-terminal kinase (JNK). The JNK activator anisomycin significantly promoted autophagy, whereas the inhibitor SP600125 markedly suppressed autophagic activation in pre-osteoclasts. Microcomputed tomography (CT), immunohistochemistry (IHC), and immunofluorescence (IF) were used to analyze the results in vivo. Consistent with the in vitro results, we found that the administration of SFN could decrease the number of osteoclasts and the expression of autophagic light chain 3 (LC3) and protect against lipopolysaccharide (LPS)-induced calvarial erosion. Our findings highlight autophagy as a crucial mechanism of SFN-mediated anti-osteoclastogenesis and show that the JNK signaling pathway participates in this process.
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Somers, Dana J., David B. Kushner, Alexandria R. McKinnis, Dzejlana Mehmedovic, Rachel S. Flame, and Thomas M. Arnold. "Epigenetic weapons in plant-herbivore interactions: Sulforaphane disrupts histone deacetylases, gene expression, and larval development in Spodoptera exigua while the specialist feeder Trichoplusia ni is largely resistant to these effects." PLOS ONE 18, no. 10 (October 19, 2023): e0293075. http://dx.doi.org/10.1371/journal.pone.0293075.
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Cruciferous plants produce sulforaphane (SFN), an inhibitor of nuclear histone deacetylases (HDACs). In humans and other mammals, the consumption of SFN alters enzyme activities, DNA-histone binding, and gene expression within minutes. However, the ability of SFN to act as an HDAC inhibitor in nature, disrupting the epigenetic machinery of insects feeding on these plants, has not been explored. Here, we demonstrate that SFN consumed in the diet inhibits the activity of HDAC enzymes and slows the development of the generalist grazer Spodoptera exigua, in a dose-dependent fashion. After consuming SFN for seven days, the activities of HDAC enzymes in S. exigua were reduced by 50%. Similarly, larval mass was reduced by 50% and pupation was delayed by 2–5 days, with no additional mortality. Similar results were obtained when SFN was applied topically to eggs. RNA-seq analyses confirm that SFN altered the expression of thousands of genes in S. exigua. Genes associated with energy conversion pathways were significantly downregulated while those encoding for ribosomal proteins were dramatically upregulated in response to the consumption of SFN. In contrast, the co-evolved specialist feeder Trichoplusia ni was not negatively impacted by SFN, whether it was consumed in their diet at natural concentrations or applied topically to eggs. The activities of HDAC enzymes were not inhibited and development was not disrupted. In fact, SFN exposure sometimes accelerated T. ni development. RNA-seq analyses revealed that the consumption of SFN alters gene expression in T. ni in similar ways, but to a lesser degree, compared to S. exigua. This apparent resistance of T. ni can be overwhelmed by unnaturally high levels of SFN or by exposure to more powerful pharmaceutical HDAC inhibitors. These results demonstrate that dietary SFN interferes with the epigenetic machinery of insects, supporting the hypothesis that plant-derived HDAC inhibitors serve as “epigenetic weapons” against herbivores.
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Wang, Jie, Ke-yong Tian, Ying Fang, Hui-min Chang, Ya-nan Han, and Fu-quan Chen. "Sulforaphane attenuates cisplatin-induced hearing loss by inhibiting histone deacetylase expression." International Journal of Immunopathology and Pharmacology 35 (January 2021): 205873842110340. http://dx.doi.org/10.1177/20587384211034086.
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Introduction Cruciferous vegetables are a rich source of sulforaphane (SFN), which acts as a natural HDAC inhibitor (HDACi). Our previous study found that HDACi could restore histone acetyltransferase/histone deacetylase (HAT/HDAC) balance in the cochlea and attenuate gentamicin-induced hearing loss in guinea pigs. Here, we investigated the protective effect of SFN on cisplatin-induced hearing loss (CIHL). Methods Thirty rats were randomly divided into 3 equal groups: the control group, cisplatin group, and SFN+cisplatin group. Rats were injected with SFN (30 mg/kg once a day) and cisplatin (7 mg/kg twice a day) for 7 days to investigate the protective role of SFN on CIHL. We observed auditory brainstem response (ABR) threshold shifts and immunostained cochlear basilar membranes of rats. For in vitro experiments, we treated HEI-OC1 cells and rat cochlear organotypic cultures with SFN (5, 10, and 15 μM) and cisplatin (10 μM). Immunofluorescence, cell viability, and protein analysis were performed to further analyze the protective mechanism of SFN on CIHL. Results SFN (30 mg/kg once a day) decreased cisplatin (7 mg/kg twice a day)-induced ABR threshold shifts and outer hair cell loss. CCK-8 assay showed that cisplatin (10 μM) reduced the viability of HEI-OC1 cells to 42%, and SFN had a dose-dependent protective effect. In cochlear organotypic cultures, we found that SFN (10 and 15 μM) increased cisplatin (10 μM)-induced myosin 7a+ cell count and restored ciliary morphology. SFN (5, 10, and 15 μM) reversed the cisplatin (10 μM)-induced increase in HDAC2, -4, and -5 and SFN (15 μM) reversed the cisplatin (10 μM)-induced decrease in H3-Ack9 [acetyl-histone H3 (Lys9)] protein expression in HEI-OC1 cells. Neither cisplatin nor cisplatin combined with SFN affected the expression of HDAC7, or HDAC9. Conclusion SFN prevented disruption of the HAT/HDAC balance, protecting against CIHL in rats.
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Kim, Wan-Uk, Jin-Sun Kong, Seung-Ah Yoo, Hyung-Ju Yoon, Yoon-Jung Park, and Chul-Soo Cho. "NADPH quinone oxidoreductase induction by sulforaphane inhibits synovial hyperplasia and rheumatoid T cell proliferation. (50.15)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 50.15. http://dx.doi.org/10.4049/jimmunol.182.supp.50.15.
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Abstract Sulforaphane (SFN), derived from cruciferous vegetables, has been previously shown to induce phase II enzyme and to have anti-carcinogenic activity. In this study, we investigated whether SFN regulates synoviocyte hyperplasia and T cell proliferation in rheumatoid arthritis (RA). SFN induced synoviocyte apoptosis by regulating Bcl-2/Bax expression and pAkt activity. In addition, SFN dose-dependently inhibited T cell proliferation and the production of IL-17 and TNF-alpha by RA mononuclear cells stimulated with anti-CD3 antibody, but enhanced the enzyme activities of NADPH quinone oxidoreductase-1 (NQO1), a representative phase II enzyme. SFN inhibition of synoviocyte survival was abrogated by co-treatment with curcumin, an inhibitor of NQO1 or by downregulation of NQO1 transcripts. The intra-peritoneal administration of SFN to mice with type II collagen (CII)-induced arthritis suppressed arthritis severity, anti-CII antibody levels, and T cell proliferative response to CII. The productions of IL-17, TNF-alpha, IL-6, and IFN-gamma from lymph node and spleen cells of these mice also were markedly reduced by SFN treatment. Moreover, in mice with anti-CII antibody-induced arthritis, a passive model of arthritis that is independent of adaptive immunity, SFN treatment reduced arthritis severity and synovial hyperplasia. In summary, NQO1 induction by SFN was found to inhibit synoviocyte proliferation and TH17 cell activation in vitro. Moreover, the anti-arthritic and immune regulatory effects of SFN were confirmed in vivo, which suggests that SFN may offer a possible treatment option for RA.
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Kahoul, Fares, Louanes Hamzioui, and Ahmed Boutarfaia. "Structural and Electrical Properties of (1-x)Pb (Zry Ti1-y)O3-xSm(Fe3+0.5, Nb5+0.5)O3 Ceramics Prepared by Conventional Solid State Synthesis and Sintered at Low Temperature." Advances in Science and Technology 87 (October 2014): 12–17. http://dx.doi.org/10.4028/www.scientific.net/ast.87.12.
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The phase structure, microstructure and electrical properties of (1-x)Pb (ZryTi1-y)O3-xSm(Fe3+0.5,Nb5+0.5)O3(PZT–SFN) (with x = 2 %, 41%≤ y ≤57 %) piezoelectric ceramics were prepared by the conventional solid state method, and effects of SFN and the Zr/Ti ratio content on the piezoelectric properties of PZT ceramics were mainly investigated. A stable solid solution has been formed between PZT and SFN, and a morphotropic phase boundary of PZT–SFN ceramics is identified in the range of 51% ≤ y ≤55 %. The Curie temperature of PZT–SFN ceramics decreases with increasing at Zr/Ti ratio content. A higher εrvalue and a lower tanδ value are demonstrated for the PZT–SFN ceramics with y = 53 %. The PZT–SFN ceramics with y = 53 % has an enhanced electrical behavior of kp~ 61.2 %, Qm~ 104, εr~ 566, tanδ ~ 2.02 % and TC~ 370OC. As a result, PZT–SFN ceramics are promising candidate materials for the field of lead piezoelectric materials and piezoelectric device.
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Guo, Youyou, Chunyan Gong, Beier Cao, Tiantian Di, Xinxin Xu, Jingran Dong, Keying Zhao, Kai Gao, and Nana Su. "Blue Light Enhances Health-Promoting Sulforaphane Accumulation in Broccoli (Brassica oleracea var. italica) Sprouts through Inhibiting Salicylic Acid Synthesis." Plants 12, no. 17 (September 1, 2023): 3151. http://dx.doi.org/10.3390/plants12173151.
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As a vegetable with high nutritional value, broccoli (Brassica oleracea var. italica) is rich in vitamins, antioxidants and anti-cancer compounds. Glucosinolates (GLs) are one of the important functional components widely found in cruciferous vegetables, and their hydrolysate sulforaphane (SFN) plays a key function in the anti-cancer process. Herein, we revealed that blue light significantly induced the SFN content in broccoli sprouts, and salicylic acid (SA) was involved in this process. We investigated the molecular mechanisms of SFN accumulation with blue light treatment in broccoli sprouts and the relationship between SFN and SA. The results showed that the SFN accumulation in broccoli sprouts was significantly increased under blue light illumination, and the expression of SFN synthesis-related genes was particularly up-regulated by SA under blue light. Moreover, blue light considerably decreased the SA content compared with white light, and this decrease was more suppressed by paclobutrazol (Pac, an inhibitor of SA synthesis). In addition, the transcript level of SFN synthesis-related genes and the activity of myrosinase (MYR) paralleled the trend of SFN accumulation under blue light treatment. Overall, we concluded that SA participates in the SFN accumulation in broccoli sprouts under blue light.
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Sangolli, Prabhakar Mallikarjuna, and Neethu Mary George. "Small-Fiber Neuropathy." Clinical Dermatology Review 8, no. 2 (April 2024): 87–94. http://dx.doi.org/10.4103/cdr.cdr_132_22.
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Small-fiber neuropathy (SFN) develops due to the impairment of fibers responsible for mediating temperature, pain, and autonomic functions. SFN complicates a number of common diseases such as diabetes mellitus, human immunodeficiency virus, and COVID-19, and is likely to be increasingly encountered. The associated pain contributes significantly to the morbidity of these diseases. Progression is slow, and most people affected by SFN do not develop large-fiber involvement over time. However, mixed polyneuropathies often start as SFN, and SFN often coexists with large fiber–predominant neuropathy. Symptoms of SFN, including painful paresthesia and dizziness, and sedative side effects of pain medications can negatively affect the quality of life. Standardized diagnostic criteria for SFN are not fully established, and skin biopsy remains the diagnostic test considered most reliable. Autonomic testing is useful when autonomic symptoms are present along with screening for associated conditions. Treatment should be individualized to control underlying causes and alleviate pain. Early diagnosis and individualized treatment are important for controlling SFN symptoms and optimizing daily functions. Here, we review the common but increasingly ignored condition, SFN, and discuss its diagnosis and management.
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Liu, Kuo-Ching, Ting-Ying Shih, Chao-Lin Kuo, Yi-Shih Ma, Jiun-Long Yang, Ping-Ping Wu, Yi-Ping Huang, Kuang-Chi Lai, and Jing-Gung Chung. "Sulforaphane Induces Cell Death Through G2/M Phase Arrest and Triggers Apoptosis in HCT 116 Human Colon Cancer Cells." American Journal of Chinese Medicine 44, no. 06 (January 2016): 1289–310. http://dx.doi.org/10.1142/s0192415x16500725.
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Sulforaphane (SFN), an isothiocyanate, exists exclusively in cruciferous vegetables, and has been shown to possess potent antitumor and chemopreventive activity. However, there is no available information that shows SFN affecting human colon cancer HCT 116 cells. In the present study, we found that SFN induced cell morphological changes, which were photographed by contrast-phase microscopy, and decreased viability. SFN also induced G2/M phase arrest and cell apoptosis in HCT 116 cells, which were measured with flow cytometric assays. Western blotting indicated that SFN increased Cyclin A, cdk 2, Cyclin B and WEE1, but decreased Cdc 25C, cdk1 protein expressions that led to G2/M phase arrest. Apoptotic cell death was also confirmed by Annexin V/PI and DAPI staining and DNA gel electrophoresis in HCT 116 cells after exposure to SFN. The flow cytometric assay also showed that SFN induced the generation of reactive oxygen species (ROS) and Ca[Formula: see text] and decreased mitochondria membrane potential and increased caspase-8, -9 and -3 activities in HCT 116 cell. Western blotting also showed that SFN induced the release of cytochrome c, and AIF, which was confirmed by confocal microscopy examination. SFN induced ER stress-associated protein expression. Based on those observations, we suggest that SFN may be used as a novel anticancer agent for the treatment of human colon cancer in the future.
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Nakatake, Richi, Tetsuya Okuyama, Yuki Hashimoto, Morihiko Ishizaki, Hidesuke Yanagida, Hiroaki Kitade, Katsuhiko Yoshizawa, Mikio Nishizawa, and Mitsugu Sekimoto. "Sulforaphane Is Protective against Warm Ischemia/Reperfusion Injury and Partial Hepatectomy in Rats." International Journal of Molecular Sciences 25, no. 1 (January 1, 2024): 579. http://dx.doi.org/10.3390/ijms25010579.
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Sulforaphane (SFN) has various beneficial effects on organ metabolism. However, whether SFN affects inflammatory mediators induced by warm hepatic ischemia/reperfusion injury (HIRI) is unclear. To investigate the hepatoprotective effects of SFN using an in vivo model of HIRI and partial hepatectomy (HIRI + PH), rats were subjected to 15 min of hepatic ischemia with blood inflow occlusion, followed by 70% hepatectomy and release of the inflow occlusion. SFN (5 mg/kg) or saline was randomly injected intraperitoneally 1 and 24 h before ischemia. Alternatively, ischemia was prolonged for 30 min to evaluate the effect on mortality. The influence of SFN on the associated signaling pathways was analyzed using the interleukin 1β (IL-1β)-treated primary cultured rat hepatocytes. In the HIRI + PH-treated rats, SFN reduced serum liver enzyme activities and the frequency of pathological liver injury, such as apoptosis and neutrophil infiltration. SFN suppressed tumor necrosis factor-alpha (TNF-α) mRNA expression and inhibited nuclear factor-kappa B (NF-κB) activation by HIRI + PH. Mortality was significantly reduced by SFN. In IL-1β-treated hepatocytes, SFN suppressed the expression of inflammatory cytokines and NF-κB activation. Taken together, SFN may have hepatoprotective effects in HIRI + PH in part by inhibiting the induction of inflammatory mediators, such as TNF-α, via the suppression of NF-κB in hepatocytes.
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Geerts, Margot, Janneke G. J. Hoeijmakers, Brigitte A. B. Essers, Ingemar S. J. Merkies, Catharina G. Faber, and Mariëlle E. J. B. Goossens. "Patient satisfaction and patient accessibility in a small fiber neuropathy diagnostic service in the Netherlands: A single-center, prospective, survey-based cohort study." PLOS ONE 19, no. 4 (April 16, 2024): e0298881. http://dx.doi.org/10.1371/journal.pone.0298881.
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Introduction Small fiber neuropathy (SFN) is a common cause of neuropathic pain in peripheral neuropathies. Good accessibility of diagnostics and treatment is necessary for an accurate diagnosis and treatment of SFN. Evidence is lacking on the quality performance of the diagnostic SFN service in the Netherlands. Our aim was to determine the patient satisfaction and -accessibility of the diagnostic SFN service, and to identify areas for improvement. Methods In a single-center, prospective, survey-based cohort study, 100 visiting patients were asked to fill in the SFN patient satisfaction questionnaire (SFN-PSQ), with 10 domains and 51 items. Cut-off point for improvement was defined as ≥ 25% dissatisfaction on an item. A chi-square test and linear regression analyses was used for significant differences and associations of patient satisfaction. Results From November 2020 to May 2021, 98 patients with SFN-related complaints filled in the online SFN-PSQ within 20 minutes. In 84% of the patients SFN was confirmed, average age was 55.1 (52.5–57.8) years and 67% was female. High satisfaction was seen in the domains ‘Waiting List Period’, Chest X-ray’, ‘Consultation with the Doctor or Nurse Practitioner (NP)’, ‘Separate Consultation with the Doctor or NP about Psychological Symptoms’, and ‘General’ of the SFN service. Overall average patient satisfaction score was 8.7 (IQR 8–10) on a 1-to-10 rating scale. Main area for improvement was shortening the 8-week period for receiving the results of the diagnostic testing (p < 0.05). General health status was statistically significant associated with patient satisfaction (p < 0.05) Conclusion A good reflection of the high patient satisfaction and -accessibility of the SFN-service is shown, with important points for improvement. These results could help hospitals widely to optimize the logistic and diagnostic pathway of SFN analysis, benchmarking patient satisfaction results among the hospitals, and to improve the quality of care of comparable SFN services.
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Flossdorf, Pia, Walter F. Haupt, Anna Brunn, Martina Deckert, Gereon R. Fink, Helmar C. Lehmann, and Gilbert Wunderlich. "Long-Time Course of Idiopathic Small Fiber Neuropathy." European Neurology 79, no. 3-4 (2018): 161–65. http://dx.doi.org/10.1159/000487717.
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Background: Small fiber neuropathy (SFN) is a challenging subtype of peripheral neuropathies. Once the diagnosis has been established, there is an uncertainty how SFN may progress, whether larger fibers will become involved over time, whether quality of life may be compromised, or whether repeated diagnostic workup in patients with unknown underlying cause may increase the yield of treatable causes of SFN. Methods: We evaluated 16 patients with documented long-time course of idiopathic SFN. Results: Clinical and electrophysiological course remained stable in 75% of the patients, while 25% SFN-patients developed large fiber neuropathies. Conclusions: Our data suggest that SFN represents a benign disease course in the majority of patients without severely limiting the quality of life.
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Palliyaguru, Dushani L., Li Yang, Dionysios V. Chartoumpekis, Stacy G. Wendell, Marco Fazzari, John J. Skoko, Yong Liao, Steffi Oesterreich, George K. Michalopoulos, and Thomas W. Kensler. "Sulforaphane Diminishes the Formation of Mammary Tumors in Rats Exposed to 17β-Estradiol." Nutrients 12, no. 8 (July 30, 2020): 2282. http://dx.doi.org/10.3390/nu12082282.
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Elevated levels of estrogen are a risk factor for breast cancer. In addition to inducing DNA damage, estrogens can enhance cell proliferation as well as modulate fatty acid metabolism that collectively contributes to mammary tumorigenesis. Sulforaphane (SFN) is an isothiocyanate derived from broccoli that is currently under evaluation in multiple clinical trials for prevention of several diseases, including cancer. Previous studies showed that SFN suppressed DNA damage and lipogenesis pathways. Therefore, we hypothesized that administering SFN to animals that are co-exposed to 17β-estradiol (E2) would prevent mammary tumor formation. In our study, 4–6 week old female August Copenhagen Irish rats were implanted with slow-release E2 pellets (3 mg x 3 times) and gavaged 3x/week with either vehicle or 100 μmol/kg SFN for 56 weeks. SFN-treated rats were protected significantly against mammary tumor formation compared to vehicle controls. Mammary glands of SFN-treated rats showed decreased DNA damage while serum free fatty acids and triglyceride species were 1.5 to 2-fold lower in SFN-treated rats. Further characterization also showed that SFN diminished expression of enzymes involved in mammary gland lipogenesis. This study indicated that SFN protects against breast cancer development through multiple potential mechanisms in a clinically relevant hormonal carcinogenesis model.
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Jun, Se-Ran, Amrita Cheema, Chhanda Bose, Marjan Boerma, Philip T. Palade, Eugenia Carvalho, Sanjay Awasthi, and Sharda P. Singh. "Multi-Omic Analysis Reveals Different Effects of Sulforaphane on the Microbiome and Metabolome in Old Compared to Young Mice." Microorganisms 8, no. 10 (September 29, 2020): 1500. http://dx.doi.org/10.3390/microorganisms8101500.
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Dietary factors modulate interactions between the microbiome, metabolome, and immune system. Sulforaphane (SFN) exerts effects on aging, cancer prevention and reducing insulin resistance. This study investigated effects of SFN on the gut microbiome and metabolome in old mouse model compared with young mice. Young (6–8 weeks) and old (21–22 months) male C57BL/6J mice were provided regular rodent chow ± SFN for 2 months. We collected fecal samples before and after SFN administration and profiled the microbiome and metabolome. Multi-omics datasets were analyzed individually and integrated to investigate the relationship between SFN diet, the gut microbiome, and metabolome. The SFN diet restored the gut microbiome in old mice to mimic that in young mice, enriching bacteria known to be associated with an improved intestinal barrier function and the production of anti-inflammatory compounds. The tricarboxylic acid cycle decreased and amino acid metabolism-related pathways increased. Integration of multi-omic datasets revealed SFN diet-induced metabolite biomarkers in old mice associated principally with the genera, Oscillospira, Ruminococcus, and Allobaculum. Collectively, our results support a hypothesis that SFN diet exerts anti-aging effects in part by influencing the gut microbiome and metabolome. Modulating the gut microbiome by SFN may have the potential to promote healthier aging.
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Ali Khan, Munawwar, Madhumitha Kedhari Sundaram, Amina Hamza, Uzma Quraishi, Dian Gunasekera, Laveena Ramesh, Payal Goala, et al. "Sulforaphane Reverses the Expression of Various Tumor Suppressor Genes by Targeting DNMT3B and HDAC1 in Human Cervical Cancer Cells." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/412149.
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Sulforaphane (SFN) may hinder carcinogenesis by altering epigenetic events in the cells; however, its molecular mechanisms are unclear. The present study investigates the role of SFN in modifying epigenetic events in human cervical cancer cells, HeLa. HeLa cells were treated with SFN (2.5 µM) for a period of 0, 24, 48, and 72 hours for all experiments. After treatment, expressions of DNMT3B, HDAC1, RARβ, CDH1, DAPK1, and GSTP1 were studied using RT-PCR while promoter DNA methylation of tumor suppressor genes (TSGs) was studied using MS-PCR. Inhibition assays of DNA methyl transferases (DNMTs) and histone deacetylases (HDACs) were performed at varying time points. Molecular modeling and docking studies were performed to explore the possible interaction of SFN with HDAC1 and DNMT3B. Time-dependent exposure to SFN decreases the expression of DNMT3B and HDAC1 and significantly reduces the enzymatic activity of DNMTs and HDACs. Molecular modeling data suggests that SFN may interact directly with DNMT3B and HDAC1 which may explain the inhibitory action of SFN. Interestingly, time-dependent reactivation of the studied TSGs via reversal of methylation in SFN treated cells correlates well with its impact on the epigenetic alterations accumulated during cancer development. Thus, SFN may have significant implications for epigenetic based therapy.
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Zhao, Zhihong, Guixiang Liao, Qin Zhou, Daoyuan Lv, Harry Holthfer, and Hequn Zou. "Sulforaphane Attenuates Contrast-Induced Nephropathy in Rats via Nrf2/HO-1 Pathway." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/9825623.
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Background. Oxidative stress plays an important role in the pathogenesis of contrast-induced nephropathy (CIN). The aim of this study was to investigate the antioxidant effects of sulforaphane (SFN) in a rat model of CIN and a cell model of oxidative stress in HK2 cells.Methods. Rats were randomized into four groups (n=6per group): control group, Ioversol group (Ioversol-induced CIN), Ioversol + SFN group (CIN rats pretreated with SFN), and SFN group (rats treated with SFN). Renal function tests, malondialdehyde (MDA), and reactive oxygen species (ROS) were measured. Western blot, real-time polymerase chain reaction analysis, and immunohistochemical analysis were performed for nuclear factor erythroid-derived 2-like 2 (Nrf2) and heme oxygenase-1 (HO-1) detection.Results. Serum blood urea nitrogen (BUN), creatinine, and renal tissue MDA were increased after contrast exposure. Serum BUN, creatinine, and renal tissue MDA were decreased in the Ioversol + SFN group as compared with those in the Ioversol group. SFN increased the expression of Nrf2 and HO-1 in CIN rats and in Ioversol-induced injury HK2 cells. SFN increased cell viability and attenuated ROS level in vitro.Conclusions. SFN attenuates experimental CIN in vitro and in vivo. This effect is suggested to activate the Nrf2 antioxidant defenses pathway.
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Li, Xiude, Yihan Wang, Guoping Zhao, Guangmin Liu, Pengjie Wang, and Jinwang Li. "Microorganisms—An Effective Tool to Intensify the Utilization of Sulforaphane." Foods 11, no. 23 (November 23, 2022): 3775. http://dx.doi.org/10.3390/foods11233775.
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Sulforaphane (SFN) was generated by the hydrolysis of glucoraphanin under the action of myrosinase. However, due to the instability of SFN, the bioavailability of SFN was limited. Meanwhile, the gut flora obtained the ability to synthesize myrosinase and glucoraphanin, which could be converted into SFN in the intestine. However, the ability of microorganisms to synthesize myrosinase in the gut was limited. Therefore, microorganisms with myrosinase synthesis ability need to be supplemented. With the development of research, microorganisms with high levels of myrosinase synthesis could be obtained by artificial selection and gene modification. Researchers found the SFN production rate of the transformed microorganisms could be significantly improved. However, despite applying transformation technology and regulating nutrients to microorganisms, it still could not provide the best efficiency during generating SFN and could not accomplish colonization in the intestine. Due to the great effect of microencapsulation on improving the colonization ability of microorganisms, microencapsulation is currently an important way to deliver microorganisms into the gut. This article mainly analyzed the possibility of obtaining SFN-producing microorganisms through gene modification and delivering them to the gut via microencapsulation to improve the utilization rate of SFN. It could provide a theoretical basis for expanding the application scope of SFN.
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Bouranis, John A., Carmen P. Wong, Laura M. Beaver, Sandra L. Uesugi, Ethan M. Papenhausen, Jaewoo Choi, Edward W. Davis, et al. "Sulforaphane Bioavailability in Healthy Subjects Fed a Single Serving of Fresh Broccoli Microgreens." Foods 12, no. 20 (October 15, 2023): 3784. http://dx.doi.org/10.3390/foods12203784.
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Cruciferous vegetable consumption is associated with numerous health benefits attributed to the phytochemical sulforaphane (SFN) that exerts antioxidant and chemopreventive properties, among other bioactive compounds. Broccoli sprouts, rich in SFN precursor glucoraphanin (GRN), have been investigated in numerous clinical trials. Broccoli microgreens are similarly rich in GRN but have remained largely unexplored. The goal of this study was to examine SFN bioavailability and the microbiome profile in subjects fed a single serving of fresh broccoli microgreens. Eleven subjects participated in a broccoli microgreens feeding study. Broccoli microgreens GRN and SFN contents and stability were measured. Urine and stool SFN metabolite profiles and microbiome composition were examined. Broccoli microgreens had similar GRN content to values previously reported for broccoli sprouts, which was stable over time. Urine SFN metabolite profiles in broccoli microgreens-fed subjects were similar to those reported previously in broccoli sprouts-fed subjects, including the detection of SFN-nitriles. We also reported the detection of SFN metabolites in stool samples for the first time. A single serving of broccoli microgreens did not significantly alter microbiome composition. We showed in this study that broccoli microgreens are a significant source of SFN. Our work provides the foundation for future studies to establish the health benefits of broccoli microgreens consumption.
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Chan, Amanda C. Y., Kathleen Ong, Jonathan J. Y. Ong, Vijay K. Sharma, Hiu Yi Wong, and Joy Vijayan. "Biomarkers in small fiber neuropathy." Exploration of Neuroprotective Therapy 2, no. 6 (December 30, 2022): 264–83. http://dx.doi.org/10.37349/ent.2022.00033.
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Small fiber neuropathy (SFN) is a relatively common, but largely understudied neurological syndrome which has affected the lives of many globally. The common symptoms of SFN include pain, dysesthesia, and autonomic dysfunction, which are caused by damage to small nerve fibers. Due to its heterogeneous nature, SFN causes a multitude of symptoms which makes the disease and its subtypes difficult to diagnose. Furthermore, as the pathophysiology of SFN remains largely enigmatic, no cause is found in around 50% of the cases and these are classified as idiopathic SFN (iSFN). The difficult task of diagnosing SFN, and the even more elusive feat of hunting for the underlying etiology, demands accurate, precise, preferably noninvasive, and affordable tools, or a combination of them. Accordingly, appropriate biomarkers for SFN are needed to stratify patients and develop cause-centered treatments in addition to symptomatic treatments. As peripheral axons grow and repair, identifying underlying causes of SFN and intervening early may spur axonal regeneration in young patients, which can greatly improve their symptoms and improve quality of life. This narrative review aims to objectively highlight functional, histological, and molecular biomarkers to aid clinicians in discerning the diagnostic tests they should use to diagnose, confirm and determine the etiology of SFN. The strengths and limitations of each potential biomarker will be discussed. Clearer diagnostic criteria, guidelines, and work-up for SFN are required for clinicians to better identify the disease in patients presenting with non-specific symptoms.
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Lee, In-Chul, and Jong-Sup Bae. "Suppressive Effects of Sulforaphane on TGFBIp-mediated Sepsis." Natural Product Communications 12, no. 10 (October 2017): 1934578X1701201. http://dx.doi.org/10.1177/1934578x1701201026.
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Sulforaphane (SFN) is produced when the enzyme myrosinase transforms glucoraphanin upon damage to the plant such as from chewing and effective in preventing carcinogenesis, diabetes, and inflammatory responses. Transforming growth factor β-induced protein (TGFBIp) is an extracellular matrix protein whose expression in several cell types is greatly increased by TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs) and functions as a mediator of experimental sepsis. We hypothesized that SFN could reduce TGFBIp-mediated severe inflammatory responses in human endothelial cells and mice. Here, we investigated the anti-septic effects and underlying mechanisms of SFN against TGFBIp-mediated septic responses. SFN effectively inhibited lipopolysaccharide-induced release of TGFBIp and suppressed TGFBIp-mediated septic responses. In addition, SFN suppressed cecal ligation and puncture (CLP)-induced sepsis lethality and pulmonary injury. In conclusion, SFN suppressed TGFBIp-mediated and CLP-induced septic responses. Therefore, SFN could be a potential therapeutic agent for treatment of various severe vascular inflammatory diseases via inhibition of the TGFBIp signaling pathway.
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Ruhee, Ruheea Taskin, and Katsuhiko Suzuki. "The Immunomodulatory Effects of Sulforaphane in Exercise-Induced Inflammation and Oxidative Stress: A Prospective Nutraceutical." International Journal of Molecular Sciences 25, no. 3 (February 1, 2024): 1790. http://dx.doi.org/10.3390/ijms25031790.
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Sulforaphane (SFN) is a promising molecule for developing phytopharmaceuticals due to its potential antioxidative and anti-inflammatory effects. A plethora of research conducted in vivo and in vitro reported the beneficial effects of SFN intervention and the underlying cellular mechanisms. Since SFN is a newly identified nutraceutical in sports nutrition, only some human studies have been conducted to reflect the effects of SFN intervention in exercise-induced inflammation and oxidative stress. In this review, we briefly discussed the effects of SFN on exercise-induced inflammation and oxidative stress. We discussed human and animal studies that are related to exercise intervention and mentioned the underlying cellular signaling mechanisms. Since SFN could be used as a potential therapeutic agent, we mentioned briefly its synergistic attributes with other potential nutraceuticals that are associated with acute and chronic inflammatory conditions. Given its health-promoting effects, SFN could be a prospective nutraceutical at the forefront of sports nutrition.
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Su, Ya, Zhe Liu, and Xiaojuan Ban. "Symmetric Face Normalization." Symmetry 11, no. 1 (January 16, 2019): 96. http://dx.doi.org/10.3390/sym11010096.
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Image registration is an important process in image processing which is used to improve the performance of computer vision related tasks. In this paper, a novel self-registration method, namely symmetric face normalization (SFN) algorithm, is proposed. There are three contributions in this paper. Firstly, a self-normalization algorithm for face images is proposed, which normalizes a face image to be reflection symmetric horizontally. It has the advantage that no face model needs to be built, which is always severely time-consuming. Moreover, it can be considered as a pre-processing procedure which greatly decreases the parameters needed to be adjusted. Secondly, an iterative algorithm is designed to solve the self-normalization algorithm. Finally, SFN is applied to the between-image alignment problem, which results in the symmetric face alignment (SFA) algorithm. Experiments performed on face databases show that the accuracy of SFN is higher than 0.95 when the translation on the x-axis is lower than 15 pixels, or the rotation angle is lower than 18°. Moreover, the proposed SFA outperforms the state-of-the-art between-image alignment algorithm in efficiency (about four times) without loss of accuracy.
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Yuan, Jian-Min, Thomas W. Kensler, Sanja Dacic, Douglas J. Harman, Renwei Wang, Paula Balogh, Lindsey Seigh, et al. "Abstract 749: Randomized placebo-controlled phase II clinical trial on oral supplementation of sulforaphane for 12 months that reduced bronchial Ki-67 index in former smokers at high risk for lung cancer." Cancer Research 84, no. 6_Supplement (March 22, 2024): 749. http://dx.doi.org/10.1158/1538-7445.am2024-749.
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Abstract Background: Epidemiological studies showed higher intake of cruciferous vegetables or their active compounds, isothiocyanates (ITCs), with lower risk of lung cancer. ITCs inhibited tobacco-carcinogen induced lung adenocarcinoma in animal models, along with reduced cellular proliferative marker Ki-67 and increased apoptotic markers Caspase-3 and TUNEL. However, human data lack. The aim of our study was to assess if oral intake of sulforaphane (SFN) for 12 months would stop/reverse the progression of bronchial histopathology, reduce Ki-67 index and/or increase Caspase-3 and TUNEL indices. Methods: A randomized clinical trial (NCT03232138) was conducted in former smokers with ≥ 30 pack-years and quitting smoking for 1-10 years in USA. Forty-three subjects were randomly assigned to the SFN (n = 21) or placebo group (n = 22) in 2018-2022. Each participant was instructed to take 4 Avmacol® or identical placebo capsules BID for 12 months. Each Avmacol® capsule contained 15 mg of glucoraphanin, which yielded a daily internal dose of 120 μmol SFN. Biopsies were collected from 6 predetermined bronchial sites at baseline and the end of treatment, respectively. The primary outcomes were the average changes of histopathology scores, Ki-67, Caspase-3 and TUNEL indices in post- vs. pre-treatment biopsies. Results: Thirty-seven participants completed the study. In the SFN group (n = 17) at baseline, 13 were men, all white, mean age 64.1 (SD 5.3) years, body mass index (BMI) 30.6 (6.1) kg/m2, years of smoking 39.5 (8.2), cigarettes per day (CPD) 23.8 (10.7), and years of quitting smoking 4.3 (2.9). The corresponding figures in the placebo group (n=20) were 9 men, 19 white, age 68.0 (3.2), BMI 28.6 (4.2), years of smoking 42.2 (4.5), CPD 25.5 (8.4), and years of quitting smoking 6.8 (3.2). The baseline medians of total Ki-67 positive nuclei were 22.3 nuclei/mm2 in the SFN group and 22.9/mm2 in the placebo group (p = 0.96). After treatment, the number of positive Ki-67 nuclei decreased by 5.3/mm2 (-24%) in the SFN group and increased by 18.0/mm2 (+79%) in the placebo group (p = 0.014) with adjustment for baseline Ki-67 and other covariates. The post- and pre-treatment difference was even greater in high-density (3+) positive Ki-67, with -46% decrease in the SFN group vs. +99% increase in the placebo group (p = 0.004). There was a dose-response effect of higher compliance with SFN intake on reducing Ki-67 index (ptrend = 0.01). SFN treatment had no impact on Caspase-3, TUNEL, or bronchial histopathology. No severe adverse event was observed in the SFN group. Conclusion: Daily intake of 120 μmol SFN for 12 months significantly reduced Ki-67 index in bronchial tissue. The findings support the potential chemopreventive effect of SFN against lung cancer development in high-risk former smokers (Grant # R01CA213123). Citation Format: Jian-Min Yuan, Thomas W. Kensler, Sanja Dacic, Douglas J. Harman, Renwei Wang, Paula Balogh, Lindsey Seigh, Yen T-H Pham, Jennifer Adams-Haduch, Shivendra Singh, James G. Herman, Avrum Spira, David O. Wilson. Randomized placebo-controlled phase II clinical trial on oral supplementation of sulforaphane for 12 months that reduced bronchial Ki-67 index in former smokers at high risk for lung cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 749.
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Huang, Yan-Bing, Hui Zheng, Xiu-Xia Yang, Cheng-Cheng Yang, Ye Liu, and Yang Liu. "Inhibition of TGF-β2-induced migration and epithelial-mesenchymal transition in ARPE-19 by sulforaphane." International Journal of Ophthalmology 14, no. 7 (July 18, 2021): 973–80. http://dx.doi.org/10.18240/ijo.2021.07.03.
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AIM: To investigate the effects of sulforaphane (SFN) on transforming growth factor (TGF)-β2 stimulated migration and epithelial-mesenchymal transition (EMT) in ARPE-19 cells. METHODS: ARPE-19 cells were cultured in the presence or absence of SFN or TGF-β2. SFN toxicity was assessed by performing a lactate dehydrogenase assay (LDH) and 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assays, and cell migration was evaluated by Transwell migration assay. Actin stress fiber formation in ARPE-19 cells was determined using immunofluorescence analysis. Immunoblotting analysis was used to determine fibronectin and α-smooth muscle actin expressions along with the degree of Smad and Akt phosphorylation. RESULTS: SFN inhibited ARPE-19 migration. Additionally, SFN attenuated TGF-β2-induced appearance of actin stress fibers as well as fibronectin and α-smooth muscle actin expressions in these cells. SFN also hindered the TGF-β2-stimulated phosphorylation of Smad2, Smad3, and Akt. SFN showed no cytotoxicity towards ARPE-19 cells. CONCLUSION: SFN inhibits TGF-β2-stimulated migration and EMT in ARPE-19 cells, probably by preventing the establishment of actin stress fibers and Akt and Smad2/3 signaling.
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Otoo, Raymond A., and Antiño R. Allen. "Sulforaphane’s Multifaceted Potential: From Neuroprotection to Anticancer Action." Molecules 28, no. 19 (October 1, 2023): 6902. http://dx.doi.org/10.3390/molecules28196902.
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Sulforaphane (SFN) is a naturally occurring compound found in cruciferous vegetables such as broccoli and cauliflower. It has been widely studied for its potential as a neuroprotective and anticancer agent. This review aims to critically evaluate the current evidence supporting the neuroprotective and anticancer effects of SFN and the potential mechanisms through which it exerts these effects. SFN has been shown to exert neuroprotective effects through the activation of the Nrf2 pathway, the modulation of neuroinflammation, and epigenetic mechanisms. In cancer treatment, SFN has demonstrated the ability to selectively induce cell death in cancer cells, inhibit histone deacetylase, and sensitize cancer cells to chemotherapy. SFN has also shown chemoprotective properties through inhibiting phase I metabolizing enzymes, modulating phase II xenobiotic-metabolizing enzymes, and targeting cancer stem cells. In addition to its potential as a therapeutic agent for neurological disorders and cancer treatment, SFN has shown promise as a potential treatment for cerebral ischemic injury and intracranial hemorrhage. Finally, the ongoing and completed clinical trials on SFN suggest potential therapeutic benefits, but more research is needed to establish its effectiveness. Overall, SFN holds significant promise as a natural compound with diverse therapeutic applications.
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Hung, Chao-Ming, Tai-Hsin Tsai, Kuan-Ting Lee, and Yi-Chiang Hsu. "Sulforaphane-Induced Cell Mitotic Delay and Inhibited Cell Proliferation via Regulating CDK5R1 Upregulation in Breast Cancer Cell Lines." Biomedicines 11, no. 4 (March 23, 2023): 996. http://dx.doi.org/10.3390/biomedicines11040996.
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Our research has revealed that sulforaphane (SFN) has chemopreventive properties and could be used in chemotherapy treatments. Further investigation is needed to understand the mechanisms behind sulforaphane’s (SFN) antitumor activity in breast adenocarcinoma, as observed in our studies. This research looked into the effects of SFN on mitosis delay and cell cycle progression in MDA-MB-231 and ZR-75-1 cells, two types of triple-negative breast cancer adenocarcinoma.The proliferation of the cancer cells after SFN exposure was evaluated using MTT assay, DNA content and cell cycle arrest induction by flow cytometry, and expressions of cdc25c, CDK1, cyclin B1 and CDK5R1 were assessed through qRT-PCR and Western blot analysis. SFN was found to inhibit the growth of cancer cells. The accumulation of G2/M-phase cells in SFN-treated cells was attributed to CDK5R1. The disruption of the CDC2/cyclin B1 complex suggested that SFN may have antitumor effects on established breast adenocarcinoma cells. Our findings suggest that, in addition to its chemopreventive properties, SFN could be used as an anticancer agent for breast cancer, as it was found to inhibit growth and induce apoptosis of cancer cells.
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He, Canxia, Luigina P. Buongiorno, Wei Wang, Jonathan C. Y. Tang, Natalizia Miceli, Maria Fernanda Taviano, Yujuan Shan, and Yongping Bao. "The Inhibitory Effect of Sulforaphane on Bladder Cancer Cell Depends on GSH Depletion-Induced by Nrf2 Translocation." Molecules 26, no. 16 (August 13, 2021): 4919. http://dx.doi.org/10.3390/molecules26164919.
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Sulforaphane (SFN), an isothiocyanate (ITCs) derived from glucosinolate that is found in cruciferous vegetables, has been reported to exert a promising anticancer effect in a substantial amount of scientific research. However, epidemical studies showed inconsistencies between cruciferous vegetable intake and bladder cancer risk. In this study, human bladder cancer T24 cells were used as in vitro model for revealing the inhibitory effect and its potential mechanism of SFN on cell growth. Here, a low dose of SFN (2.5 µM) was shown to promote cell proliferation (5.18–11.84%) and migration in T24 cells, whilst high doses of SFN (>10 µM) inhibited cell growth significantly. The induction effect of SFN on nuclear factor (erythroid-derived 2)-like 2 (Nrf2) expression at both low (2.5 µM) and high dose (10 µM) was characterized by a bell-shaped curve. Nrf2 and glutathione (GSH) might be the underlying mechanism in the effect of SFN on T24 cell growth since Nrf2 siRNA and GSH-depleting agent L-Buthionine-sulfoximine abolished the effect of SFN on cell proliferation. In summary, the inhibitory effect of SFN on bladder cancer cell growth and migration is highly dependent on Nrf2-mediated GSH depletion and following production. These findings suggested that a higher dose of SFN is required for the prevention and treatment of bladder cancer.
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Silva, Bruna L. R., Gisele Simão, Carmem D. L. Campos, Cinara R. A. V. Monteiro, Laryssa R. Bueno, Gabriel B. Ortis, Saulo J. F. Mendes, et al. "In Silico and In Vitro Analysis of Sulforaphane Anti-Candida Activity." Antibiotics 11, no. 12 (December 19, 2022): 1842. http://dx.doi.org/10.3390/antibiotics11121842.
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Oropharyngeal candidiasis/candidosis is a common and recurrent opportunistic fungal infection. Fluconazole (FLZ), one of the most used and effective antifungal agents, has been associated with a rise of resistant Candida species in immunocompromised patients undergoing prophylactic therapy. Sulforaphane (SFN), a compound from cruciferous vegetables, is an antimicrobial with yet controversial activities and mechanisms on fungi. Herein, the in silico and antifungal activities of SFN against C. albicans were investigated. In silico analyzes for the prediction of the biological activities and oral bioavailability of SFN, its possible toxicity and pharmacokinetic parameters, as well as the estimates of its gastrointestinal absorption, permeability to the blood-brain barrier and skin, and similarities to drugs, were performed by using different software. SFN in vitro anti-Candida activities alone and in combination with fluconazole (FLZ) were determined by the broth microdilution method and the checkerboard, biofilm and hyphae formation tests. Amongst the identified probable biological activities of SFN, nine indicated an antimicrobial potential. SFN was predicted to be highly absorbable by the gastrointestinal tract, to present good oral availability, and not to be irritant and/or hepatotoxic. SFN presented antifungal activity against C. albicans and prevented both biofilm and hyphae formation by this microorganism. SFN was additive/synergistic to FLZ. Overall, the data highlights the anti-Candida activity of SFN and its potential to be used as an adjuvant therapy to FLZ in clinical settings.
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Mu, Yang, Tai-lang Yin, Xiao-xuan Huang, Xue Hu, Lu Yin, and Jing Yang. "Sulforaphane ameliorates high-fat diet-induced spermatogenic deficiency in mice†." Biology of Reproduction 101, no. 1 (April 20, 2019): 223–34. http://dx.doi.org/10.1093/biolre/ioz067.
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Abstract Sulforaphane (SFN), a dietary isothiocyanate that is mainly found in cruciferous vegetables, possesses anti-oxidative and anticancer activity and modulates inflammation. However, little is known about the role of SFN in obesity-related male reproductive defects. The present study aimed to investigate the effects of SFN on high-fat diet (HFD)-induced male spermatogenic impairment and further clarify the possible underlying mechanisms. In this study, 8-week-old mice were randomly divided into four groups. Mice were fed a normal diet or an HFD with or without SFN supplementation. Sulforaphane was subcutaneously injected at a dose of 0.5 mg/kg 5 days/week for 4 weeks beginning 8 weeks after initiation of the HFD. The results demonstrated that SFN could protect against HFD-induced reproductive dysfunction in male mice. Moreover, SFN also improved reproductive ability, as demonstrated by an increased pregnancy rate and decreased embryo resorption rate in comparison to the corresponding HFD group. We also observed a decrease in apoptosis and an attenuation of endoplasmic reticulum (ER) stress after SFN treatment. In vitro studies of mouse and human sperm samples also revealed that SFN protects against the palmitic acid-induced reduction in sperm viability and motility by inhibiting ER stress in an AMP-activated protein kinase (AMPK)-dependent manner. AMPK-dependent ER stress attenuation by SFN was further confirmed using AMPK knockout mice. Taken together, these data show that SFN protects against HFD-induced male reproductive dysfunction by inhibiting ER stress and apoptosis. These findings may be helpful for identifying new therapeutic methods to treat male infertility.
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Abbas, Ata, J. Adam Hall, William L. Patterson, Emily Ho, Anna Hsu, Fahd Al-Mulla, and Philippe T. Georgel. "Sulforaphane modulates telomerase activity via epigenetic regulation in prostate cancer cell lines." Biochemistry and Cell Biology 94, no. 1 (February 2016): 71–81. http://dx.doi.org/10.1139/bcb-2015-0038.
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Epidemiologic studies have revealed that diets rich in sulforaphane (SFN), an isothiocyanate present in cruciferous vegetables, are associated with a marked decrease in prostate cancer incidence. The chemo-preventive role of SFN is associated with its histone de-acetylase inhibitor activity. However, the effect of SFN on chromatin composition and dynamic folding, especially in relation to HDAC inhibitor activity, remains poorly understood. In this study, we found that SFN can inhibit the expression and activity of human telomerase reverse transcriptase (hTERT), the catalytic subunit of telomerase, in 2 prostate cancer cell lines. This decrease in gene expression is correlated with SFN-induced changes in chromatin structure and composition. The SFN-mediated changes in levels of histone post-translational modifications, more specifically acetylation of histone H3 lysine 18 and di-methylation of histone H3 lysine 4, 2 modifications linked with high risk of prostate cancer recurrence, were associated with regulatory elements within the hTERT promoter region. Chromatin condensation may also play a role in SFN-mediated hTERT repression, since expression and recruitment of MeCP2, a known chromatin compactor, were altered in SFN treated prostate cancer cells. Chromatin immuno-precipitation (ChIP) of MeCP2 showed enrichment over regions of the hTERT promoter with increased nucleosome density. These combined results strongly support a role for SFN in the mediation of epigenetic events leading to the repression of hTERT in prostate cancer cells. This ability of SFN to modify chromatin composition and structure associated with target gene expression provides a new model by which dietary phytochemicals may exert their chemoprevention activity.
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Wan, Xiang, Chong Liu, Yan-Bo Chen, Meng Gu, Zhi-Kang Cai, Qi Chen, and Zhong Wang. "Sulforaphane Treatment of Stress Urinary Incontinence Via the Nrf2-ARE Pathway in a Rat Model." Cellular Physiology and Biochemistry 44, no. 5 (2017): 1912–22. http://dx.doi.org/10.1159/000485880.
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Background/Aims: To explore the effect of sulforaphane (SFN) treatment in rats through the induction of Stress Urinary Incontinence (SUI) via the Nrf2-ARE pathway. Methods: A total of 18 female rats (Sprague-Dawley) were assigned to three groups: a control group, an SUI group, and an SUI+SFN group (six rats per group). Rats in the treatment groups were induced via postpartum vaginal balloon dilation and bilateral ovariectomy. Rats in the SUI+SFN group were treated via intraperitoneal injection once per day for a total of one month. Urethral sphincter muscle histological was observed by HE and Masson staining. Peak voiding pressure and interval of micturition were measured by cystometry. Oxidative stress markers and protein expression in the Nrf2-ARE pathway were examined by immunohistochemical staining and western blotting. Results: Prolonged micturition interval and higher peak voiding pressure were observed in the SUI+SFN group. Disturbance of muscle morphology was ameliorated, muscle content was elevated, and collagen content was restrained in response to SFN treatment. The SOD, GSH-Px, and CAT activities were elevated in the SUI+SFN group compared to those in the control group. The level of cell apoptosis was decreased in SUI rats after SFN treatment; however, apoptosis was mainly located in the urethral mucosa instead of the muscle layer. SFN reduced the Bax/Bcl-2 expression ratio. Nrf2 and Nrf2 target antioxidant proteins were elevated in the SFN group. Conclusions: SFN was effective for SUI treatment via decreasing oxidative stress and activating the Nrf2-ARE pathway.
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Huo, Li, Yu Su, Gaoyang Xu, Lingling Zhai, and Jian Zhao. "Sulforaphane Protects the Male Reproductive System of Mice from Obesity-Induced Damage: Involvement of Oxidative Stress and Autophagy." International Journal of Environmental Research and Public Health 16, no. 19 (October 7, 2019): 3759. http://dx.doi.org/10.3390/ijerph16193759.
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(1) Background: In recent decades, the prevalence of obesity has grown rapidly worldwide, thus causing many diseases, including male hypogonadism. Sulforaphane (SFN), an isothiocyanate compound, has been reported to protect the reproductive system. This research investigated the protective effect of SFN against obesity-induced impairment in the male reproductive system and explored the potential mechanism involved in mice. (2) Methods: One hundred thirty mice were divided into 5 groups (Control, DIO (diet-induced obesity), DIO + SFN 5 mg/kg, DIO + SFN 10 mg/kg, and DIO + SFN 20 mg/kg). The effects of SFN on the male reproductive system were determined based on the sperm count and motility, relative testes and epididymis weights, hormone levels, and pathological analyses. Oxidative stress was determined by measuring malondialdehyde (MDA), total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione (GSH), H2O2, catalase (CAT), and glutathione peroxidase (GSH-PX) levels. Protein expression of nuclear factor erythroid-2 related factor 2 (Nrf2), Kelch-like ECH-associated protein-1 (Keap1), Microtubule-associated protein light chain 3 (LC3), Beclin1, and P62 were determined by western blotting. (3) Results: High-fat diet (HFD)-induced obesity significantly decreased relative testes and epididymis weights, sperm count and motility, and testosterone levels but increased leptin and estradiol levels. SFN supplementation ameliorated these effects. Additionally, SFN administration inhibited the obesity-induced MDA accumulation and increased the SOD level. Western blot indicated that SFN had an important role in the downregulation of Keap1. Moreover, SFN treatment attenuated obesity-induced autophagy, as detected by LC3 and Beclin1. (4) Conclusions: SFN ameliorated the reproductive toxicity associated with obesity by inhibiting oxidative stress mediated by the nuclear factor erythroid-2 related factor 2/ antioxidant response element (Nrf2/ARE) signaling pathway and recovery of normal autophagy.
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Ruhee, Ruheea Taskin, and Katsuhiko Suzuki. "The Integrative Role of Sulforaphane in Preventing Inflammation, Oxidative Stress and Fatigue: A Review of a Potential Protective Phytochemical." Antioxidants 9, no. 6 (June 13, 2020): 521. http://dx.doi.org/10.3390/antiox9060521.
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Cruciferous vegetables hold a myriad of bioactive molecules that are renowned for possessing unique medicinal benefits. Sulforaphane (SFN) is one of the potential nutraceuticals contained within cruciferous vegetables that is useful for improving health and diseased conditions. The objective of this review is to discuss the mechanistic role for SFN in preventing oxidative stress, fatigue, and inflammation. Direct and indirect research evidence is reported to identify the nontoxic dose of SFN for human trials, and effectiveness of SFN to attenuate inflammation and/or oxidative stress. SFN treatment modulates redox balance via activating redox regulator nuclear factor E2 factor-related factor (Nrf2). SFN may play a crucial role in altering the Keap1/Nrf2/ARE pathway (an intricate response to many stimuli or stress), which induces Nrf2 target gene activation to reduce oxidative stress. In addition, SFN reduces inflammation by suppressing centrally involved inflammatory regulator nuclear factor-kappa B (NF-κB), which in turn downregulates the expression of proinflammatory cytokines and mediators. Exercise may induce a significant range of fatigue, inflammation, oxidative stress, and/or organ damage due to producing excessive reactive oxygen species (ROS) and inflammatory cytokines. SFN may play an effective role in preventing such damage via inducing phase 2 enzymes, activating the Nrf2/ARE signaling pathway or suppressing nuclear translocation of NF-κB. In this review, we summarize the integrative role of SFN in preventing fatigue, inflammation, and oxidative stress, and briefly introduce the history of cruciferous vegetables and the bioavailability and pharmacokinetics of SFN reported in previous research. To date, very limited research has been conducted on SFN’s effectiveness in improving exercise endurance or performance. Therefore, more research needs to be carried out to determine the effectiveness of SFN in the field of exercise and lifestyle factors.
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Tomooka, Fumimasa, Kosuke Kaji, Norihisa Nishimura, Takahiro Kubo, Satoshi Iwai, Akihiko Shibamoto, Junya Suzuki, et al. "Sulforaphane Potentiates Gemcitabine-Mediated Anti-Cancer Effects against Intrahepatic Cholangiocarcinoma by Inhibiting HDAC Activity." Cells 12, no. 5 (February 22, 2023): 687. http://dx.doi.org/10.3390/cells12050687.
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Intrahepatic cholangiocarcinoma (iCCA), the second most common primary liver cancer, has high mortality rates because of its limited treatment options and acquired resistance to chemotherapy. Sulforaphane (SFN), a naturally occurring organosulfur compound found in cruciferous vegetables, exhibits multiple therapeutic properties, such as histone deacetylase (HDAC) inhibition and anti-cancer effects. This study assessed the effects of the combination of SFN and gemcitabine (GEM) on human iCCA cell growth. HuCCT-1 and HuH28 cells, representing moderately differentiated and undifferentiated iCCA, respectively, were treated with SFN and/or GEM. SFN concentration dependently reduced total HDAC activity and promoted total histone H3 acetylation in both iCCA cell lines. SFN synergistically augmented the GEM-mediated attenuation of cell viability and proliferation by inducing G2/M cell cycle arrest and apoptosis in both cell lines, as indicated by the cleavage of caspase-3. SFN also inhibited cancer cell invasion and decreased the expression of pro-angiogenic markers (VEGFA, VEGFR2, HIF-1α, and eNOS) in both iCCA cell lines. Notably, SFN effectively inhibited the GEM-mediated induction of epithelial–mesenchymal transition (EMT). A xenograft assay demonstrated that SFN and GEM substantially attenuated human iCCA cell-derived tumor growth with decreased Ki67+ proliferative cells and increased TUNEL+ apoptotic cells. The anti-cancer effects of every single agent were markedly augmented by concomitant use. Consistent with the results of in vitro cell cycle analysis, G2/M arrest was indicated by increased p21 and p-Chk2 expression and decreased p-Cdc25C expression in the tumors of SFN- and GEM-treated mice. Moreover, treatment with SFN inhibited CD34-positive neovascularization with decreased VEGF expression and GEM-induced EMT in iCCA-derived xenografted tumors. In conclusion, these results suggest that combination therapy with SFN with GEM is a potential novel option for iCCA treatment.