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1
Dell'Agli, Mario, Omar Maschi, Germana V. Galli, Rossana Fagnani, Esther Dal Cero, Donatella Caruso, and Enrica Bosisio. "Inhibition of platelet aggregation by olive oil phenols via cAMP-phosphodiesterase." British Journal of Nutrition 99, no. 5 (May 2008): 945–51. http://dx.doi.org/10.1017/s0007114507837470.
Анотація:
The aim of the present study was to confirm that olive oil phenols reduce human platelet aggregability and to verify the hypothesis that cAMP- and cGMP- phosphodiesterases (PDE) could be one of the targets of the biological effect. Four extracts from oils characterized by a high phenol content (HPE), and low phenol levels (LPE) were prepared and analyzed quali- and quantitatively by HPLC-UV and electrospray ionization–MS/MS. Human washed platelets stimulated with thrombin were used for the aggregation assay. Human platelet cAMP-PDE and recombinant PDE5A1 were used as enzyme source. Platelet aggregation and enzyme activity were assayed in the presence of HPE, LPE and individual phenols. The phenol content of HPE ranged between 250 and 500 mg/kg, whereas the LPE content was 46 mg/kg. The compounds identified were hydroxytyrosol (HT), tyrosol (TY), oleuropein aglycone (OleA) and the flavonoids quercetin (QU), luteolin (LU) and apigenin (AP). OleA was the most abundant phenol (range 23·3 to 37·7 %) and LU was the most abundant flavonoid in the extracts. Oil extracts inhibited platelet aggregation with an 50% inhibitory concentration interval of 1·23–11·2 μg/ml. The inhibitory effect of individual compounds (10 μm) including homovanillyl alcohol (HVA) followed this order: OleA>LU>HT = TY = QU = HVA, while AP was inactive. All the extracts inhibited cAMP-PDE, while no significant inhibition of PDE5A1 (50μg/ml) was observed. All the flavonoids and OleA inhibited cAMP-PDE, whereas HT, TY, HVA (100 μm) were inactive. Olive oil extracts and part of its phenolic constituents inhibit platelet aggregation; cAMP-PDE inhibition is one mechanism through which olive oil phenols inhibit platelet aggregation.
2
Li, Daowen, Xingyao Pei, Xiaoling Qin, Xinyu Liu, Cun Li, Liuan Li, Chongshan Dai, Xilong Xiao, and Shusheng Tang. "Olaquindox-Induced Liver Damage Involved the Crosstalk of Oxidative Stress and p53 In Vivo and In Vitro." Oxidative Medicine and Cellular Longevity 2020 (December 18, 2020): 1–18. http://dx.doi.org/10.1155/2020/8835207.
Анотація:
Olaquindox (OLA), a member of the quinoxaline-N,N-dioxide family, has been widely used as a growth-promoting feed additive and treatment for bacterial infections. The toxicity has been a major concern, and the precise molecular mechanism remains poorly understood. The present study was aimed at investigating the roles of oxidative stress and p53 in OLA-caused liver damage. In a mouse model, OLA administration could markedly cause liver injury as well as the induction of oxidative stress and activation of p53. Antioxidant N-acetylcysteine (NAC) inhibited OLA-induced oxidative stress and p53 activation in vivo. Furthermore, knockout of the p53 gene could significantly inhibit OLA-induced liver damage by inhibiting oxidative stress and the mitochondria apoptotic pathway, compared to the p53 wild-type liver tissue. The cell model in vitro further demonstrated that p53 knockout or knockdown in the HCT116 cell and L02 cell significantly inhibited cell apoptosis and increased cell viability, presented by suppressing ROS production, oxidative stress, and the Nrf2/HO-1 pathway. Moreover, loss of p53 decreased OLA-induced mitochondrial dysfunction and caspase activations, with the evidence of inhibited activation of phosphorylation- (p-) p38 and p-JNK and upregulated cell autophagy via activation of the LC3 and Beclin1 pathway in HCT116 and L02 cells. Taken together, our findings provided a support that p53 primarily played a proapoptotic role in OLA-induced liver damage against oxidative stress and mitochondrial dysfunction, which were largely dependent on suppression of the JNK/p38 pathway and upregulation of the autophagy pathway via activation of LC3 and Beclin1.
3
Song, Chaoran, Deok Jeong, Yo Han Hong, Wan Yi Li, Sang Woo Lee, Mohammad Amjad Hossain, Amani Taamalli, Ji Hye Kim, Jong-Hoon Kim та Jae Youl Cho. "Anti-Inflammatory and Photoaging-Protective Effects of Olea europaea through Inhibition of AP-1 and NF-κ B Pathways". American Journal of Chinese Medicine 48, № 08 (січень 2020): 1895–913. http://dx.doi.org/10.1142/s0192415x20500950.
Анотація:
Olea europaea is a beneficial edible plant with a number of biological activities like anti-inflammatory, anti-oxidant, antithrombic, antihyperglycemic, and anti-ischemic activities. The mechanisms behind the antiphotoaging and anti-inflammatory effects of Olea europaea are not fully understood. To investigate how an ethanol extract of Olea europaea (Oe-EE) exerts these effects, we explored its activities in human keratinocytes and dermal fibroblasts. We assessed the anti-oxidant effects of Oe-EE via 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2[Formula: see text]-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) assays and measured the expression levels of matrix metalloproteinases (MMPs), cyclooxygenase-2, interleukin (IL)-6, tumor necrosis factor (TNF)-[Formula: see text], and moisturizing factors. Antiphotoaging and anti-inflammatory mechanisms of Oe-EE were explored by assessing signaling molecule activation via immunoblotting. Oe-EE treatment decreased the mRNA expression level of MMPs, cyclooxygenase-2, IL-6, and TNF-[Formula: see text] and restored type I collagen, filaggrin, and sirtuin 1 expression in UVB-irradiated cells. Furthermore, Oe-EE inhibited the activities of several activator protein 1 regulatory enzymes, including extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), and inhibited nuclear factor (NF)-[Formula: see text]B pathway signaling proteins. Therefore, our results indicate that Oe-EE has photoaging-protective and anti-inflammatory effects.
4
Aumeeruddy, Muhammad Zakariyyah, and Mohamad Fawzi Mahomoodally. "Ethnomedicinal Plants for the Management of Diabetes Worldwide: A Systematic Review." Current Medicinal Chemistry 28, no. 23 (August 2, 2021): 4670–93. http://dx.doi.org/10.2174/0929867328666210121123037.
Анотація:
Background: The increasing incidence of diabetes worldwide has urged researchers to explore novel antidiabetic agents from natural products. Ethnomedicinal field studies on diabetes have expanded across the globe, documenting large numbers of folk medicinal plants against diabetes. Nonetheless, a systematic review of these surveys has not been conducted so far. This study documents the medicinal plants traditionally used globally for managing diabetes. Methods: Key databases including Sciencedirect, Medline/PubMed, and Google Scholar were scrutinized. The Plant List and The International Plant Names Index (IPNI) were used to validate the scientific plant names. Results: 2004 traditionally used plants belonging to 1112 genera and 197 families were reported across 92 countries for the management of diabetes. Leguminosae (105 genera and 193 species), Compositae (97 genera and 188 species), and Lamiaceae (47 genera and 121 species) were the main plant families reported. Momordica charantia L., Syzygium cumini (L.) Skeels, Allium sativum L., Azadirachta indica A.Juss., Catharanthus roseus (L.) G.Don, Olea europaea L., Trigonella foenum-graecum L., Gymnema sylvestre (Retz.) R.Br. ex Sm., Aloe vera (L.) Burm.f., and Allium cepa L were the species mostly reported. Indeed, the antidiabetic properties of these main species have been evidenced by experimental studies. Several antidiabetic compounds acting via different mechanisms have been identified, including momordicoside, karaviloside, cucurbitacin, charantin, and charantoside from M. charantia, cuminoside from S. cumini, S-allyl cysteine sulfoxide from A. sativum, limonoids from A. indica, alkaloids including vindoline, vindolidine, vindolicine and vindolinine from C. roseus, oleuropein and oleanolic acid from O. europaea, flavone C-glycosides such as vicenin-1, isoschaftoside, and schaftoside from T. foenum-graecum seeds, gymnemosides, gymnemagenin, and pregnane glycosides from G. sylvestre, chysalodin from A. vera, and quercetin from A. cepa. Conclusion: This review is the first to provide a compiled list of traditional medicinal plants used worldwide against diabetes.
5
Bao, Jiapeng, Weifeng Yan, Kai Xu, Mengyao Chen, Zhonggai Chen, Jisheng Ran, Yan Xiong, Lidong Wu та Ratanesh K. Seth. "Oleanolic Acid Decreases IL-1β-Induced Activation of Fibroblast-Like Synoviocytes via the SIRT3-NF-κB Axis in Osteoarthritis". Oxidative Medicine and Cellular Longevity 2020 (28 вересня 2020): 1–10. http://dx.doi.org/10.1155/2020/7517219.
Анотація:
Synovial inflammation is a major pathological feature of osteoarthritis (OA), which is a chronic degenerative joint disease. Fibroblast-like synoviocytes (FLS), localized in the synovial membrane, are specialized secretory cells. During OA synovitis, FLS produce chemokines and cytokines that stimulate chondrocytes to secrete inflammatory cytokines and activate matrix metalloproteinases (MMPs) in FLS. Recent studies have demonstrated that sirtuin 3 (SIRT3) performs as a key regulator in maintaining mitochondrial homeostasis in OA. This study aims at ascertaining whether SIRT3 is involved in OA synovitis. The overexpression (OE) and knockdown (KD) of SIRT3 are established by short hairpin RNA (shRNA) and recombinant plasmid in human FLS. The anti-inflammatory effect of SIRT3 underlying in oleanolic acid- (OLA-) prevented interleukin-1β- (IL-1β-) induced FLS dysfunction is then evaluated in vitro. Additionally, the molecular mechanisms of SIRT3 are assessed, and the interaction between SIRT3 and NF-κB is investigated. The data suggested that SIRT3 can be detected in human synovial tissues during OA, and OLA could elevate SIRT3 expression. OE-SIRT3 and OLA exhibited equal authenticity to repress inflammation and reverse oxidative stress changes in IL-1β-induced human FLS dysfunction. KD-SIRT3 was found to exacerbate inflammation and oxidative stress changes in human FLS. Furthermore, it was found that SIRT3 could directly bind with NF-κB, resulting in the suppression of NF-κB activation induced by IL-1β in human FLS, which then repressed synovial inflammation in OA. In general, the activation of SIRT3 by OLA inhibited synovial inflammation by suppressing the NF-κB signal pathway in FLS, and this suggested that SIRT3 is a potential target for OA synovitis therapy.
6
El-Hamoly, Tarek, Zoltán Hajnády, Máté Nagy-Pénzes, Edina Bakondi, Zsolt Regdon, Máté A. Demény, Katalin Kovács, et al. "Poly(ADP-Ribose) Polymerase 1 Promotes Inflammation and Fibrosis in a Mouse Model of Chronic Pancreatitis." International Journal of Molecular Sciences 22, no. 7 (March 30, 2021): 3593. http://dx.doi.org/10.3390/ijms22073593.
Анотація:
Chronic pancreatitis (CP) is an inflammatory disease of the pancreas characterized by ductal obstructions, tissue fibrosis, atrophy and exocrine and endocrine pancreatic insufficiency. However, our understanding is very limited concerning the disease’s progression from a single acute inflammation, via recurrent acute pancreatitis (AP) and early CP, to the late stage CP. Poly(ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor enzyme activated mostly by oxidative DNA damage. As a co-activator of inflammatory transcription factors, PARP1 is a central mediator of the inflammatory response and it has also been implicated in acute pancreatitis. Here, we set out to investigate whether PARP1 contributed to the pathogenesis of CP. We found that the clinically used PARP inhibitor olaparib (OLA) had protective effects in a murine model of CP induced by multiple cerulein injections. OLA reduced pancreas atrophy and expression of the inflammatory mediators TNFα and interleukin-6 (IL-6), both in the pancreas and in the lungs. Moreover, there was significantly less fibrosis (Masson’s trichrome staining) in the pancreatic sections of OLA-treated mice compared to the cerulein-only group. mRNA expression of the fibrosis markers TGFβ, smooth muscle actin (SMA), and collagen-1 were markedly reduced by OLA. CP was also induced in PARP1 knockout (KO) mice and their wild-type (WT) counterparts. Inflammation and fibrosis markers showed lower expression in the KO compared to the WT mice. Moreover, reduced granulocyte infiltration (tissue myeloperoxidase activity) and a lower elevation of serum amylase and lipase activity could also be detected in the KO mice. Furthermore, primary acinar cells isolated from KO mice were also protected from cerulein-induced toxicity compared to WT cells. In summary, our data suggest that PARP inhibitors may be promising candidates for repurposing to treat not only acute but chronic pancreatitis as well.
7
Tezcan, G., SA Aksoy, B. Tunca, A. Bekar, M. Mutlu, G. Cecener, U. Egeli, H. Kocaeli, H. Demirci, and MO Taskapilioglu. "Oleuropein modulates glioblastoma miRNA pattern different from Olea europaea leaf extract." Human & Experimental Toxicology 38, no. 9 (June 6, 2019): 1102–10. http://dx.doi.org/10.1177/0960327119855123.
Анотація:
Glioblastoma (GBM) is the most prevalent and deadliest subtype of glioma. Despite current innovations in existing therapeutic modalities, GBM remains incurable, and alternative therapies are required. Previously, we demonstrated that Olea europaea leaf extract (OLE) kills GBM cells by modulating miR-181b, miR-137, miR-153 and Let-7d expression. However, although oleuropein (OL) is the main compound in OLE, its role in the antitumour effect of OLE remains unknown. This study determined the effect of OL on GBM cell line T98G and compared the results with our previous findings regarding the effect of OLE on the same cell line. The antiproliferative activity of OL and its effect on temozolomide (TMZ) response were tested inT98G cells using WST-1 assay. OL inhibition was evaluated using one-way analysis of variance with Tukey’s post hoc test. The effect of OL on miR-181b, miR-137, miR-153 and Let-7d expression was assessed using quantitative reverse transcription polymerase chain reaction. Fold differences in expression between untreated, OL or OL + TMZ-treated samples were calculated using 2−ΔCt method. Significance was evaluated using an independent sample t-test. Treatment with 277.5 and 555 µM OL resulted in 39.51% and 75.40% reductions in T98G cells within 24 h. Coadministration of 325 µM TMZ and 277.5 or 555 µM, OL caused 2.08- and 2.83-fold increases, respectively, in the therapeutic effect of TMZ. OL + TMZ significantly increased microRNA expression, particularly Let-7d, than OLE. In conclusion, OL has an antitumour effect on GBM cells mainly via regulation of Let-7d expression. The present results also indicate other minor compounds in OLE play important anticancer roles.
8
Misra, Ranjita, Bamadeb Patra, Sudha Varadharaj, and Rama Shanker Verma. "Establishing the promising role of novel combination of triple therapeutics delivery using polymeric nanoparticles for Triple negative breast cancer therapy." BioImpacts 11, no. 3 (July 31, 2020): 199–207. http://dx.doi.org/10.34172/bi.2021.27.
Анотація:
Introduction: Triple-negative breast cancer (TNBC) is a lethal tumor with an advanced degree of metastasis and poor survivability as compared to other subtypes of breast cancer. TNBC which consists of 15 % of all types of breast cancer is categorized by the absence of expression of estrogen receptors (ER), progesterone receptors (PR) and human epidermal growth factor receptor-2 (HER2). This is the main reason for the failure of current hormonal receptor-based therapies against TNBCs, thus leading to poor patient outcomes. Therefore, there is a necessity to develop novel therapies targeting this devastating disease. Methods: In this study, we have targeted TNBC by simultaneous activation of apoptosis through DNA damage via cytotoxic agent such as paclitaxel (PAC), inhibition of PARP activity via PARP inhibitor, olaparib (OLA) and inhibiting the activity of FOXM1 proto-oncogenic transcription factor by using RNA interference technology (FOXM1-siRNA) in nanoformulations. Experiments conducted in this investigation include cellular uptake, cytotoxicity and apoptosis study using MDA-MB-231 cells. Results: The present study validates that co-delivery of two drugs (PAC and OLA) along with FOXM1-siRNA by cationic NPs, enhances the therapeutic outcome leading to greater cytotoxicity in TNBC cells. Conclusion: The current investigation focuses on designing a multifunctional drug delivery platform for concurrent delivery of either PAC or PARP inhibitor (olaparib) and FOXM1 siRNA in chitosan-coated poly(D, L-lactide-co-glycolide) (PLGA) nanoparticles (NPs) with the ability to emerge as a front runner therapeutic for TNBC therapy.
9
Qiu, Mingning, Jie Liu, Yongxia Su, Rong Guo, Baoyu Zhao, and Jianjun Liu. "Diosmetin Induces Apoptosis by Downregulating AKT Phosphorylation via P53 Activation in Human Renal Carcinoma ACHN Cells." Protein & Peptide Letters 27, no. 10 (November 2, 2020): 1022–28. http://dx.doi.org/10.2174/0929866527666200330172646.
Анотація:
Background: Diosmetin (DIOS) is the aglycone of the flavonoid glycoside, diosmin, derived naturally from the leaves of the legume, Olea europaea, and Acacia farnesiana. It has potent anticancer activity against multiple forms of cancers. However, the role of DIOS in renal carcinoma and its mechanism of action remain unclear. Objective: The purpose of this study is to investigate the effect of DIOS on cell viability and apoptosis in renal carcinoma cells and explore the possible mechanism of action. Methods: Cell viability, cytotoxicity, caspase activity, apoptosis, and expression of apoptotic related proteins were analyzed in renal carcinoma ACHN cells. Results: The results showed that DIOS inhibited the cell viability, and induced cytotoxicity and apoptosis in ACHN cells. Furthermore, DIOS increased expression of p53 mRNA and proteins, and downregulated phosphorylation of the phosphoinositide 3-kinase and protein B kinase (PI3K/AKT). In addition, it was observed that the anticancer effect of DIOS was significantly enhanced by the p53 activator, but inhibited by the p53 inhibitor. Conclusion: Our data suggested that DIOS induced apoptosis in renal carcinoma ACHN cells by reducing AKT phosphorylation through p53 upregulation.
10
De la Ossa, Felice, Azimi, Salsano, Digiacomo, Macchia, Danti, and Di Stefano. "Waste Autochthonous Tuscan Olive Leaves (Olea europaea var. Olivastra seggianese) as Antioxidant Source for Biomedicine." International Journal of Molecular Sciences 20, no. 23 (November 25, 2019): 5918. http://dx.doi.org/10.3390/ijms20235918.
Анотація:
Olive leaf extract (OLE) can be obtained as biowaste and is extensively used a food supplement and an over-the-counter drug for its beneficial effects. New studies have investigated OLE concerning the role of oxidative stress in the pathogenesis of vascular disease. This in vitro study aims to evaluate if OLE extracted from the Tuscan Olea europaea protects endothelial cells against oxidative stress generated by reactive oxygen species (ROS). Methods: OLE total polyphenols (TPs) were characterized by the Folin–Ciocalteu method. Endothelial cells were grown in conventional cultures (i.e., two-dimensional, 2D) and on a biomaterial scaffold (i.e., three-dimensional, 3D) fabricated via electrospinning. Cell viability and ROS measurement after H2O2 insults were performed. Results: OLE TP content was 23.29 mg GAE/g, and oleuropein was the principal compound. The dose-dependent viability curve highlighted the absence of significant cytotoxic effects at OLE concentrations below 250 µg/mL TPs. By using OLE preconditioning at 100 µg/mL, cell viability decrease was observed, being in 3D lower than in the 2D model. OLE was protective against ROS in both models. Conclusions: OLE represents a high-value antioxidant source obtained by biowaste that is interesting for biomedical products. Using a 3D scaffold could be the best predictive model to mimic the physiological conditions of vascular tissue reaction.
11
Limam, Inès, Mohamed Abdelkarim, Rym Essid, Ahlem Chahbi, Mayssa Fathallah, Salem Elkahoui, and Fatma Ben Aissa-Fennira. "Olea europaea L. cv. Chetoui leaf and stem hydromethanolic extracts suppress proliferation and promote apoptosis via caspase signaling on human multiple myeloma cells." European Journal of Integrative Medicine 37 (August 2020): 101145. http://dx.doi.org/10.1016/j.eujim.2020.101145.
12
Zeriouh, Wafa, Abdelhafid Nani, Meriem Belarbi, Adélie Dumont, Charlotte de Rosny, Ikram Aboura, Fatima Zahra Ghanemi, et al. "Phenolic extract from oleaster (Olea europaea var. Sylvestris) leaves reduces colon cancer growth and induces caspase-dependent apoptosis in colon cancer cells via the mitochondrial apoptotic pathway." PLOS ONE 12, no. 2 (February 17, 2017): e0170823. http://dx.doi.org/10.1371/journal.pone.0170823.
13
Rungarunlert, S., N. Klincumhom, C. Nemes, M. Techakumphu, M. K. Pirity, and A. Dinnyes. "293 MASS PRODUCTION OF Nkx2.5-POSITIVE CARDIAC PROGENITOR CELLS DERIVED FROM MOUSE EMBRYONIC STEM CELLS IN SLOW-TURNING LATERAL VESSEL FOR CELL TRANSPLANTATION AND DRUG TESTING." Reproduction, Fertility and Development 23, no. 1 (2011): 244. http://dx.doi.org/10.1071/rdv23n1ab293.
Анотація:
Regenerative cell therapy against cardiovascular disease would require mass production and purification of specific cell types before transplantation. To enable large-scale production of embryonic stem (ES)-derived pure cardiomyocytes, we developed an animal model for a single-step scalable bioprocess that allows direct embryoid body (EB) formation in a fully controlled slow-turning lateral vessel (STLV, Synthecon, Inc., Houston, TX, USA) bioreactor following inoculation with a single cell suspension of mouse ES cells. To enhance the yield of cardiac progenitor cells, mouse ES cells (HM1; 129Sv/Ola, Magin et al. 1992 Nucl. Acids Res. 20, 3795–3796) were targeted with the cardiac-specific mouse Nkx2.5 promoter driven enhanced fluorescent green protein (EGFP). Among 15 targeted colonies, which were characterised based on morphology, the ability to form EB, EGFP expression, and in vitro differentiation ability toward cardiomyocytes, 3 lines were further evaluated for the efficiency of cardiomyocyte production. The 3 lines were cultured in STLV bioreactor and compared with classical hanging drop (HD) and static suspension culture methods. Embryonic bodies at day 3 to 8 were collected and analysed by using fluorescence-activated cell sorting for markers of pluripotency (e.g. Oct-4, SSEA1, Nanog) and cardiac (e.g. Nkx2.5, Troponin T) lineage commitments. Data was analysed by one-way ANOVA and t-tests. The results showed that both level and kinetics of Nkx2.5 expression was dependent on culture conditions. The STLV and static suspension culture methods produced higher rates of Nkx2.5-positive cells on day 5 than that of HD (70 and 54 v. 30%, respectively). The STLV method produced a highly uniform population of efficiently differentiating EB in large quantities and resulted in the highest, 108 yield of cardiomyocytes in a single 110-mL STLV on day 4. In conclusion, the STLV method provides a technological platform for controlled large-scale generation of ES-cell-derived cardiomyocytes for clinical and industrial applications. In vivo transplantation tests of cardiomyocytes produced via STLV are currently underway. This study was financed by EU FP6 (CLONET, MRTN-CT-2006-035468), EU FP7 (PartnErS, PIAP-GA-2008-218205; InduHeart, PEOPLE-IRG-2008-234390; InduStem, PIAP-GA-2008-230675; PluriSys, HEALTH-2007-B-223485); NKTH-OTKA-EU FP7-HUMAN-2009-MB08-C 80205 and NKTH/KPI (NKFP_07_1-ES2HEART-HU OM-00202-2007), CHE-TRF senior scholarship, No. RTA 5080010 (M.T.), and the Thailand Commission on Higher Education [CHE-PhD-SW-2005-100 (S.R.), CHE-PhD-SW-RG-2007 (N.K.)].
14
Bräuner, E. V., T. Koch, A. Juul, D. A. Doherty, R. Hart, and M. Hickey. "Prenatal exposure to maternal stressful life events and earlier age at menarche: the Raine Study." Human Reproduction 36, no. 7 (March 21, 2021): 1959–69. http://dx.doi.org/10.1093/humrep/deab039.
Анотація:
Abstract STUDY QUESTION Is there an association between prenatal exposure to stressful life events and age at menarche, and does childhood BMI mediate this association? SUMMARY ANSWER Girls exposed to prenatal stress had a slightly earlier age at menarche, but this association did not show a dose-response effect and was not mediated by childhood offspring BMI. WHAT IS ALREADY KNOWN Prenatal stress may impact on reproductive function in females including age at menarche, but human data are very limited. High childhood BMI is known to be associated with earlier age at menarche. Only one small study has measured the association between maternal stress and age at menarche and reported that childhood BMI mediated the association between maternal stress and earlier age at menarche. However, neither maternal stress nor age at menarche was prospectively recorded and the study was limited to 31 mother–daughter pairs. STUDY DESIGN, SIZE, DURATION The Raine Study is a large prospective population-based pregnancy cohort study (n = 1414 mother–daughter pairs) continuously followed from prenatal life through to adolescence. In the present study, we examined the association between exposure to maternal stressful life events during early, late and total gestation and age at menarche in offspring using 753 mother–daughter pairs with complete case information. PARTICIPANTS/MATERIALS, SETTING, METHODS Mothers prospectively reported stressful life events during pregnancy at 18 and 34 weeks using a standardized 10-point questionnaire. Exact date of menarche was assessed using a purpose-designed questionnaire at 8, 10, 14 and 17 years of age. Complete information on exposure, outcome and confounding variables was obtained from 753 mothers–daughter pairs. Multivariate linear regression complete case analysis was used to examine associations between maternal stressful life event exposure and age at menarche. Potential selection bias was evaluated using multiple imputations (50 datasets). The mediating effects of offspring childhood BMI (ages 5, 8, or 10 years) on these associations were measured in separate sub-analyses. MAIN RESULTS AND ROLE OF CHANCE Most (580/753, 77%) daughters were exposed to at least one prenatal stressful life event. Exposure to maternal stressful life events during the entire pregnancy was associated with a non-linear earlier age at menarche. Exposure to one event and two or more psychological stressful events was associated with a 3.5 and 1.7-month earlier onset of puberty, respectively when compared to the reference group with no exposure maternal stressful life events. The estimates from multiple imputation with 50 datasets were comparable with complete case analysis confirming the existence of an underlying effect. No separate significant effects were observed for exposure during early or late gestation. The association between prenatal stressful events and age at menarche was not mediated by childhood BMI in the offspring. LIMITATIONS, REASONS FOR CAUTION Stressful life events may have affected pregnant women in different ways and self-perceived maternal stress severity may have provided a more precise estimate of gestational psychological stress. The observed non-linear U-shape of the association between maternal psychological stress and age at menarche did not reflect a dose-response. This suggests that the first exposure to prenatal stress exerts a greater effect on fetal reproductive development. A potential mechanism is via dramatic initial activation of the hypothalamic–pituitary–adrenal (HPA) axis following the first stressful life event which is greater than that observed following subsequent exposure to two or more maternal stressful life events. Whilst we adjusted for a priori chosen confounders, we cannot exclude residual confounding or confounding by factors we did not include. Maternal age at menarche was not available so the effects of familial history/genetics could not be assessed. There was a large loss due to the number of girls with no information on date of menarche and missing confounder information implying risk of selection bias and multiple imputation analyses did not fully exclude this risk (similar direction but slightly weaker estimate magnitude). WIDER IMPLICATIONS OF THE FINDINGS Menarche is a sentinel reproductive event and earlier age at menarche carries implications for psychological, social and reproductive health and for long-term risk of common non-communicable diseases. Understanding the factors regulating age at menarche has extensive health implications. This is the first population-based cohort study in humans to demonstrate that prenatal psychological stress might directly modify age at menarche. STUDY FUNDING/COMPETING INTEREST(S) Dr. Bräuner and Trine Koch’s salaries were supported by Doctor Sofus Carl Emil Friis and spouse Olga Doris Friis foundation, The Danish Cancer Society (Kræftens Bekæmpelse, RP15468, R204-A12636, Denmark) and The Danish Health Foundation (Helsefonden, F-22181-23, Denmark). Martha Hickey was funded by NHMRC Practitioner Fellowships. The funding bodies played no role in the design, collection, analysis, or interpretation of data; in the writing of the manuscript; or in the decision to submit the manuscript for publication. Dr. Hart has received personal fees in his function as the Medical Director of Fertility Specialists of Western Australia and received educational sponsorship grants from MSD, Merck-Serono and from Ferring Pharmaceuticals. Dr Hart has also received personal fees from Shareholders in Western IVF outside the submitted work. TRIAL REGISTRATION NUMBER NA.
15
Yu, Shuang-Quan, and Donna H. Wang. "Abstract 084: Activation Of Trpv1-expressing Renal Sensory Nerves With N-oleoyldopamine Attenuates High Fat Diet-induced Impairment In Renal Function." Hypertension 64, suppl_1 (September 2014). http://dx.doi.org/10.1161/hyp.64.suppl_1.084.
Анотація:
Renal injury occurs in obesity. Accumulating evidence indicates that activation of the transient receptor potential vanilloid 1 (TRPV1) protects tissues from injury albeit the mechanisms are largely unknown. We test the hypothesis that high fat diet (HFD) intake impairs afferent renal nerves expressing TRPV1 channels, leading to increased renal sympathetic nerve activity (RSNA), decreased renal function, and hypertension, and that chronic activation of TRPV1 positive afferent renal nerves attenuates HFD-induced impairment. N-oleoyldopamine (OLDA, 1 ng/kg, daily), a selective TRPV1 agonist, was administrated intrathecally (T8-L3) via a indwelled catheter to chronically activate TRPV1 positive afferent renal nerves in rats fed a HFD or normal fat diet (Con) for 8 weeks. HFD decreased renal TRPV1 expression and afferent renal nerve activity (ARNA, Con: 133±8, Con+OLDA: 127±15, HFD: 84±5, HFD+OLDA: 115±7, p<0.05) in response to intra-pelvis perfusion of capsaicin (4 μM, 3 min, 20 ml/min), a selective TRPV1 agonist, which were prevented by OLDA. HFD increased RSNA responses to intrathecal injection of muscimol (3 nmol/kg), a GABA-A receptor agonist, and urinary norepinephrine levels, which were prevented by OLDA. HFD decreased creatinine clearance and increased urinary albumin levels, which were prevented by OLDA (Creatinine clearance, Con: 0.52±0.09, Con+OLDA: 0.54±0.12, HFD: 0.24±0.04, HFD+OLDA: 0.40±0.06 ml/min/100 gbwt, p<0.05). HFD increased levels of collagen deposition, connective tissue growth factor (CTGF), and matrix metalloproteinase-2 (MMP-2) in the kidney, which were prevented by OLDA. HFD increased systolic blood pressure by the week of 6 after HFD, which was prevented by OLDA. Thus, HFD impairs TRPV1-positive afferent renal nerves, increases renal sympathetic nerve activity, and leads to renal injury and hypertension. Segment-specific intrathecal injection of OLDA protects against HFD-induced impairment in afferent renal nerves and prevents HFD-induced renal injury and hypertension. Our data illustrate that preservation of TRPV1 positive afferent renal nerves may be a therapeutic strategy in preventing obesity- or type 2 diabetes-induced renal injury and hypertension.
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Wang, Donna H., and Beihua Zhong. "Abstract 535: Impaired Natriuresis and Increased Salt Sensitivity in Response to Acute Salt Load During Western Diet-intake: Role of Trpv1." Hypertension 62, suppl_1 (September 2013). http://dx.doi.org/10.1161/hyp.62.suppl_1.a535.
Анотація:
Western diet (WD) intake increases morbidity of obesity, diabetes, and salt sensitive hypertension albeit mechanisms are largely unknown. We tested the hypothesis that the transient receptor potential vanilloid type 1 (TRPV1) channels are activated during WD intake to protect against salt-induced increases in blood pressure possibly via enhancing natriuresis. Wild-type (WT, C57BL/6) or gene-targeted TRPV1-null mutant (TRPV1 -/- ) mice were fed a normal (CON) or Western (WD) diet for 16-18 weeks. Mean arterial pressure (MAP), determined by radiotelemetry after acute sodium loading (NS, 0.9% NaCl) or vehicle (C) by gavage with or without treatment with Nω-nitro-l-arginine methyl ester ( L - NAME, 10mg/kg, ip. ) or a TRPV1 agonist, N-oleoyldopamine ( OLDA, 0.1mg/kg, ip ), was not different between two strains fed a CON diet. WT or TRPV1-/- mice fed a WD diet had increased MAP after NS, with a greater magnitude in TRPV1-/- mice (p<0.05). OLDA decreased while L-NAME increased MAP in WT-WD-NS but not TRPV1-/-WD-NS mice (p<0.05). The urinary nitrates plus nitrites excretion (UNOx, umol*4h urine/kg BW), an indicator of renal nitric oxide (NO) production, was increased in both strains fed a CON diet after NS (p<0.05). OLDA further increased while L-NAME prevented NS-induced increases in UNOx in WT-CON-NS only or in both strains, respectively. TRPV1 ablation with WD intake decreased UNOx levels before NS and abolished NS-induced increment in UNOx (WT-WD-C: 0.3 ±0.06 vs. TRPV1-/-WD-C: 0.2 ±0.05; and WT-WD-NS: 0.7 ±0.1 vs. TRPV1-/-WD-NS: 0.3 ±0.1; p<0.05). OLDA further increased while L-NAME prevented NS-induced increment in UNOx in WT-WD-NS mice only (p<0.05). Urinary sodium excretion was increased in both strains fed a CON diet after NS (p<0.05), which was unaffected by OLDA or L-NAME. UNa was increased in WT-WD-NS but not TRPV1-/-WD-NS after NS. OLDA further increased while L-NAME prevented NS-induced increases in UNa in WT-WD-NS only. Thus, TRPV1 ablation increases salt sensitivity during WD intake possibly via impaired NS-induced renal NO production and sodium excretion. Activation of TRPV1 with OLDA enhances renal NO production and sodium excretion, resulting in prevention of increased salt sensitivity during WD intake.
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CHEN, IRIS E., Brian Tsui, Joe X. Qiao, William Hsu, Latisha K. Sharma, Mercedeh B. Hosseini, May Nour, et al. "Abstract P378: Automated Estimation of Ischemic Core Volume on Non-Contrast-Enhanced Computed Tomography via Machine Learning." Stroke 52, Suppl_1 (March 2021). http://dx.doi.org/10.1161/str.52.suppl_1.p378.
Анотація:
Background and Purpose: Accurate estimation of ischemic core on baseline imaging has treatment implications in patients with acute ischemic stroke (AIS). Machine learning (ML) algorithms have shown promising results in estimating ischemic core using routine non-contrast CT (NCCT). We used a ML-trained algorithm to quantify ischemic core volume on NCCT and compared the results to concurrent diffusion MRI as the reference standard in patients with AIS. Methods: We analyzed consecutive anterior circulation AIS patients who had baseline (pretreatment) NCCT and MRI (DWI). Ischemic lesion volume was calculated on MRI-DWI using an automated software (Olea Medical SAS, La Ciotat, France). An automatic segmentation approach using a combination of traditional 3D graphics and statistical methods, and ML classification techniques (Brainomix, Oxford, United Kingdom) was used to identify ischemic core voxels on NCCT. Total ischemic core volumes on ML-NCCT and DWI-MR were quantitatively compared by Bland-Altman plots and Pearson correlation. Results: A total of 50 patients (27 female, 23 male, mean age 72.6 years) were included. Baseline imaging was performed within 173 ± 143 minutes (mean ± SD) from symptom onset. The mean time difference between MRI and NCCT was 72 min. The baseline NIHSS was 14, 8-21 (Median, IQR). Algorithm-segmented ischemic core volume detected on NCCT was median 12.7 mL, IQR 3.5-26.0 mL. Ischemic core volume on DWI MRI was median 8.8 mL, IQR 3.2-34.0 mL. ML-NCCT core volumes significantly correlated with DWI MRI core volumes, r =0.61, p <0.001. The mean difference between the ML-NCCT and DWI MRI core volumes was 12.4 mL, p =0.81. For the reperfusion treatment threshold of an ischemic core volume within 70 mL, while no patients would have been excluded using our algorithm, five patients would have been incorrectly dichotomized as having an ischemic volume of <70 mL compared to MRI. Conclusion: This ML-approach accurately quantifies ischemic core volume on NCCT compared to the reference standard of diffusion MRI in patients with AIS.
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Oppi, S., S. Stein, V. Marzolla, E. Osto, Z. Rancic, T. F. Luscher, M. Oosterveer, and S. Stein. "P1941The nuclear receptor corepressor 1 blocks CD36-mediated foam cell formation in atherogenesis." European Heart Journal 40, Supplement_1 (October 1, 2019). http://dx.doi.org/10.1093/eurheartj/ehz748.0688.
Анотація:
Abstract Background Nuclear receptors and their cofactors regulate the expression of various target genes in different tissue and organs to orchestrate downstream (patho)physiological processes. Although the function of several nuclear receptors in atherosclerosis has been studied, very little is known about the role of nuclear receptor cofactors in atherosclerosis. Given its important role to suppress inflammatory processes, we speculated that macrophage nuclear receptor corepressor 1 (NCOR1) plays a protective function in atherosclerosis development. Purpose To evaluate the contribution of macrophage NCOR1 in atherosclerosis we used myeloid cell-specific Ncor1 knockout mice on an atherosclerosis-prone background. Methods and results 8-week-old male and female mice were exposed to a high high-cholesterol diet for 12 weeks. Our findings demonstrate that the lack of macrophage Ncor1 leads to a severe atherosclerotic phenotype in both sexes. These mice show a higher content of plaques along the thoraco-abdominal aortae as well as at the aortic sinus, which were characterized by larger necrotic cores and thinner fibrous caps, a typical signature of unstable plaques. Moreover, we found that the pro-atherogenic effects of the Ncor1 deletion are mediated via derepression of peroxisome proliferator-activated receptor gamma (PPARγ) target genes in mouse and human macrophages, especially the enhanced expression of the CD36 scavenger receptor and the subsequent rise in oxLDL uptake. Interestingly, while the expression of NCOR1 is reduced, the PPARγ signature is increased in human atherosclerotic plaques, and this signature is further pronounced in ruptured compared to stable carotid plaques. Conclusion Our findings suggest that macrophage NCOR1 blocks the pro-atherogenic functions of PPARγ in atherosclerosis and prevents the disease development. Acknowledgement/Funding The Swiss National Science Foundation, the Novartis Foundation, Olga-Mayenfisch Foundation, the OPO foundation