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1
Lee, Hyun-Su, Eun-Nam Kim, and Gil-Saeng Jeong. "Lupenone Protects Neuroblastoma SH-SY5y Cells Against Methamphetamine-Induced Apoptotic Cell Death via PI3K/Akt/mTOR Signaling Pathway." International Journal of Molecular Sciences 21, no. 5 (February 27, 2020): 1617. http://dx.doi.org/10.3390/ijms21051617.
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Methamphetamine (METH) is an addictive psychostimulant showing neurotoxicity through neuronal apoptosis and the neuro-inflammatory pathway. Lupenone, a lupane triterpenoid, is an isolated compound exhibiting anti-oxidative, anti-inflammation, and anti-diabetic activities. However, whether lupenone plays a protective role against apoptosis induced by METH in SH-SY5y neuroblastoma cells remains unknown. In the present study, we elucidated that lupenone had no toxicity to SH-SY5y cells at different concentrations. On the other hand, we found that the treatment of SH-SY5y cells with an optimal concentration of lupenone could lead to protection against cell death induced by METH. AnnexinV/PI apoptosis analysis revealed a dramatically reduced level of the apoptotic cell population in lupenon and METH treated SH-SY5y cells. Moreover, diminished expression of anti-apoptotic proteins, including Bcl-2, Caspase3, Caspase7, and Caspase8 in METH-exposed SH-SY5y cells, was significantly recovered by treatment with lupenone. This protection in the expression of anti-apoptotic proteins was due to an increased phosphorylation level of PI3K/Akt in METH-treated SH-SY5y cells pre-incubated with lupenone. These findings suggest that lupenone can protect SH-SY5y cells against METH-induced neuronal apoptosis through the PI3K/Akt pathway.
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An, Xinfang, Zixing Fu, Chendi Mai, Weiming Wang, Linyu Wei, Dongliang Li, Chaokun Li, and Lin-Hua Jiang. "Increasing the TRPM2 Channel Expression in Human Neuroblastoma SH-SY5Y Cells Augments the Susceptibility to ROS-Induced Cell Death." Cells 8, no. 1 (January 8, 2019): 28. http://dx.doi.org/10.3390/cells8010028.
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Human neuroblastoma SH-SY5Y cells are a widely-used human neuronal cell model in the study of neurodegeneration. A recent study shows that, 1-methyl-4-phenylpyridine ion (MPP), which selectively causes dopaminergic neuronal death leading to Parkinson’s disease-like symptoms, can reduce SH-SY5Y cell viability by inducing H2O2 generation and subsequent TRPM2 channel activation. MPP-induced cell death is enhanced by increasing the TRPM2 expression. By contrast, increasing the TRPM2 expression has also been reported to support SH-SY5Y cell survival after exposure to H2O2, leading to the suggestion of a protective role for the TRPM2 channel. To clarify the role of reactive oxygen species (ROS)-induced TRPM2 channel activation in SH-SY5Y cells, we generated a stable SH-SY5Y cell line overexpressing the human TRPM2 channel and examined cell death and cell viability after exposure to H2O2 in the wild-type and TRPM2-overexpressing SH-SY5Y cells. Exposure to H2O2 resulted in concentration-dependent cell death and reduction in cell viability in both cell types. TRPM2 overexpression remarkably augmented H2O2-induced cell death and reduction in cell viability. Furthermore, H2O2-induced cell death in both the wild-type and TRPM2-overexpressing cells was prevented by 2-APB, a TRPM2 inhibitor, and also by PJ34 and DPQ, poly(ADP-ribose) polymerase (PARP) inhibitors. Collectively, our results show that increasing the TRPM2 expression renders SH-SY5Y cells to be more susceptible to ROS-induced cell death and reinforce the notion that the TRPM2 channel plays a critical role in conferring ROS-induced cell death. It is anticipated that SH-SY5Y cells can be useful for better understanding the molecular and signaling mechanisms for ROS-induced TRPM2-mediated neurodegeneration in the pathogenesis of neurodegenerative diseases.
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Song, Zurong, and Ali Tao. "The Neuroprotective Effects of Astragaloside IV against H2O2-Induced Damage in SH-SY5Y Cells are Associated with Synaptic Plasticity." Journal of Chemistry 2020 (May 13, 2020): 1–7. http://dx.doi.org/10.1155/2020/5343619.
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The aim of this study was to investigate whether the neuroprotective effects of astragaloside IV (AS-IV) against hydrogen peroxide (H2O2)-induced damage on human neuroblastoma cell line (SH-SY5Y) are associated with synaptic plasticity. The concentration screening of AS-IV and H2O2 on SH-SY5Y cells and the protective effects of AS-IV on SH-SY5Y cells under H2O2 stress were all determined by MTT assay. The expression of postsynaptic density 95 (PSD-95) and growth-associated protein 43 (GAP-43) were measured by western blot (WB) and inmunofluorescence staining assay under the same treatment conditions. According to the MTT results, the concentration of H2O2 at 50 μmol/L for 3 h was used for the cell damage model, and various concentrations of AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) were used to affect SH-SY5Y cells. The MTT results showed that pretreatment of SH-SY5Y cells with AS-IV (0.1, 0.2, 0.3, and 0.4 μmol/L) attenuated the damage induced by H2O2 (50 μmol/L, 51.62% cell viability) and increased cell viability to 64.19, 63.48, 65.86, and 65.81%, respectively. Western blot analysis and immunofluorescence staining showed that the protective effects of AS-IV against SH-SY5Y cell damage caused by H2O2 resulted in reduced expression of PSD-95 and increased expression of GAP-43 in comparison with the H2O2 treatment group. The conclusion shows that AS-IV protected SH-SY5Y cells and enhanced their viability under H2O2 stress. AS-IV may facilitate presynaptic and postsynaptic plasticity to exert protective effects against oxidative damage of SH-SY5Y cells.
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Qin, Chunlian, Saisai Zhang, Qunchen Yuan, Mengxue Liu, Nan Jiang, Liujing Zhuang, Liquan Huang, and Ping Wang. "A Cell Co-Culture Taste Sensor Using Different Proportions of Caco-2 and SH-SY5Y Cells for Bitterness Detection." Chemosensors 10, no. 5 (May 5, 2022): 173. http://dx.doi.org/10.3390/chemosensors10050173.
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Bitter taste receptors (T2Rs) are involved in bitter taste perception, which is one of the five basic taste modalities in mammals. In this study, a cell co-culture taste sensor using different proportions of Caco-2 cells and SH-SY5Y cells was proposed. Caco-2 cells, which endogenously expressed the human T2R38 receptor, and SH-SY5Y cells, which endogenously expressed the human T2R16 receptor, were co-cultured. Using Caco-2 cells and SH-SY5Y cells at a constant total concentration of 40 K/mL, we designed seven mixtures with [Caco-2]/([Caco-2] + [SH-SY5Y]) ratios of 0, 20, 40, 50, 60, 80, and 100%. These mixtures were then seeded on the 16 E-plates of the electric cell-substrate impedance sensor (ECIS) for bitterness detection. Theoretically, after T2R38 ligands activation, continuous evolution profiles (CEP), with [Caco-2]/([Caco-2] + [SH-SY5Y]) ratios as the x-axis and ΔCI (Max) as the y-axis, would exhibit positive correlation property. After T2R16 ligands activation, the CEP would show negative correlation property. However, when stimulated with compounds that could activate both T2R16 and T2R38, it would show different response patterns.
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Ahmad, Faizan. "Inflammatory response of stem cell secreting conditioned media in SH-SY5Y cell line." Bionatura 5, no. 3 (August 15, 2020): 1243–45. http://dx.doi.org/10.21931/rb/2020.05.03.13.
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Mesenchymal stem cells (MSCs) are reported to secrete anti-inflammatory cytokines and growth factors, which makes MSCs a promising candidate in the treatment of various neurodegenerative diseases. SH-SY5Y show extreme inflammatory response under LPS and an inadequate inflammatory response when treated with Wharton's jelly, conditioned media. This study mainly focuses on the inflammatory (pro and anti-inflammatory) response of SH-SY5Y by gene expression study. SH-SY5Y cell line used for cell culture and RT- q PCR was done with 5 different primers. In this article, lipopolysaccharides (LPS) show a significant result in pro-inflammatory and pro-apoptotic. In this article, we focus on the therapeutic approach of stem cells, which reduce inflammation by secreting stem cell factors to cure various neurodegenerative diseases.
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Xu, Xiaonan, Chengle Zhuang, Zimu Wu, Hongyan Qiu, Haixia Feng, and Jun Wu. "LincRNA-p21 Inhibits Cell Viability and Promotes Cell Apoptosis in Parkinson’s Disease through Activating α-Synuclein Expression." BioMed Research International 2018 (December 25, 2018): 1–10. http://dx.doi.org/10.1155/2018/8181374.
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Long intergenic noncoding RNA-p21 (lincRNA-p21) has been reported to be increased in Parkinson’s disease (PD). However, the function and underlying mechanisms of lincRNA-p21 remain not clear. In order to explore the role of lincRNA-p21 in PD, we used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce in vivo PD model (C57BL/6 mice) and utilized N-methyl-4-phenylpyridinium (MPP+) to create in vitro PD model (SH-SY5Y cells). Results showed that the expression level of lincRNA-p21 was increased significantly in PD models. High abundance of lincRNA-p21 inhibited viability and promoted apoptosis markedly in SH-SY5Y cells treated with MPP+. Mechanistically, further experiments demonstrated that upregulation of lincRNA-p21 could sponge miR-1277-5p and indirectly increase the expression of α-synuclein to suppress viability and activate apoptosis in SH-SY5Y cells. In short, our study illustrated that lincRNA-p21/miR-1277-5p axis regulated viability and apoptosis in SH-SY5Y cells treated with MPP+ via targeting α-synuclein. LincRNA-p21 might be a novel target for PD.
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Pires, Ana O., Andreia Neves-Carvalho, Nuno Sousa, and António J. Salgado. "The Secretome of Bone Marrow and Wharton Jelly Derived Mesenchymal Stem Cells Induces Differentiation and Neurite Outgrowth in SH-SY5Y Cells." Stem Cells International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/438352.
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The goal of this study was to determine and compare the effects of the secretome of mesenchymal stem cells (MSCs) isolated from human bone-marrow (BMSCs) and the Wharton jelly surrounding the vein and arteries of the umbilical cord (human umbilical cord perivascular cells (HUCPVCs)) on the survival and differentiation of a human neuroblastoma cell line (SH-SY5Y). For this purpose, SH-SY5Y cells were differentiated with conditioned media (CM) from the MSCs populations referred above. Retinoic acid cultured cells were used as control for neuronal differentiated SH-SY5Y cells. SH-SY5Y cells viability assessment revealed that the secretome of BMSCs and HUCPVCs, in the form of CM, was able to induce their survival. Moreover, immunocytochemical experiments showed that CM from both MSCs was capable of inducing neuronal differentiation of SH-SY5Y cells. Finally, neurite lengths assessment and quantitative real-time reverse-transcription polymerase chain reaction (RT-PCR) analysis demonstrated that CM from BMSCs and HUCPVCs differently induced neurite outgrowth and mRNA levels of neuronal markers exhibited by SH-SY5Y cells. Overall, our results show that the secretome of both BMSCs and HUCPVCs was capable of supporting SH-SY5Y cells survival and promoting their differentiation towards a neuronal phenotype.
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Wei, Bo, Gui-rong Xiao, Cheng-long Wu, and Yi-qin Xu. "HAGLR promotes neuron differentiation through the miR-130a-3p-MeCP2 axis." Open Medicine 16, no. 1 (January 1, 2021): 1121–31. http://dx.doi.org/10.1515/med-2021-0301.
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Abstract Parkinson’s disease (PD) is a prevalent neurodegenerative disease. Currently, the molecular mechanisms underlying the progressions of PD are not fully understood. The human neuroblastoma cell line SH-SY5Y has been widely used as an in vitro model for PD. This study aims to investigate the molecular mechanisms of the non-coding RNA-mediated SH-SY5Y differentiation induced by retinoic acid (RA). By microArray analysis, lncRNA HAGLR was observed to be significantly upregulated during the RA-induced SH-SY5Y differentiation. Silencing HAGLR blocked the RA-induced SH-SY5Y differentiation. Moreover, bioinformatical analysis illustrated that miR-130a-3p contains binding sites for HAGLR. The RNA-pull down assay and luciferase assay demonstrated that HAGLR functioned as a ceRNA of miR-130a-3p in SH-SY5Y cells. Overexpression of miR-130a-3p effectively inhibited SH-SY5Y differentiation. We identified MeCP2, a vital molecule in neuronal diseases, to be a direct target of miR-130a-3p in SH-SY5Y cells by western blot and luciferase assays. The rescue experiments verified that recovery of miR-130a-3p in HAGLR-overexpressing SH-SY5Y cells could successfully overcome the RA-induced SH-SY5Y differentiation by targeting MeCP2. In summary, this study reveals a potential molecular mechanism for the lncRNA-HAGLR-promoted in vitro neuron differentiation by targeting the miR-130a-3p-MeCP2 axis, contributing to the understanding of the pathogenesis and progression of PD.
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Zhang, Yuan, Tun Sun, Meng Li, Yanling Lin, Yue Liu, Shusheng Tang, and Chongshan Dai. "Ivermectin-Induced Apoptotic Cell Death in Human SH-SY5Y Cells Involves the Activation of Oxidative Stress and Mitochondrial Pathway and Akt/mTOR-Pathway-Mediated Autophagy." Antioxidants 11, no. 5 (May 5, 2022): 908. http://dx.doi.org/10.3390/antiox11050908.
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Ivermectin (IVM) could cause potential neurotoxicity; however, the precise molecular mechanisms remain unclear. This study explores the cytotoxicity of IVM in human neuroblastoma (SH-SY5Y) cells and the underlying molecular mechanisms. The results show that IVM treatment (2.5–15 μM) for 24 h could induce dose-dependent cell death in SH-SY5Y cells. Compared to the control, IVM treatment significantly promoted the production of ROS, mitochondrial dysfunction, and cell apoptosis. IVM treatment also promoted mitophagy and autophagy, which were charactered by the decreased expression of phosphorylation (p)-Akt and p-mTOR proteins, increased expression of LC3II, Beclin1, ATG5, PINK, and Pakin1 proteins and autophagosome formation. N-acetylcysteine treatment significantly inhibited the IVM-induced production of ROS and cell death in SH-SY5Y cells. Autophagy inhibitor (e.g., 3-methyladenine) treatment significantly inhibited IVM-induced autophagy, oxidative stress, and cell apoptosis. Taken together, our results reveal that IVM could induce autophagy and apoptotic cell death in SH-SY5Y cells, which involved the production of ROS, activation of mitochondrial pathway, and inhibition of Akt/mTOR pathway. Autophagy inhibition improved IVM-induced oxidative stress and apoptotic cell death in SH-SY5Y cells. This current study provides new insights into understanding the molecular mechanism of IVM-induced neurotoxicity and facilitates the discovery of potential neuroprotective agents.
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Lavrin, Teja, Tilen Konte, Rok Kostanjšek, Simona Sitar, Kristina Sepčič, Sonja Prpar Mihevc, Ema Žagar, et al. "The Neurotropic Black Yeast Exophiala dermatitidis Induces Neurocytotoxicity in Neuroblastoma Cells and Progressive Cell Death." Cells 9, no. 4 (April 14, 2020): 963. http://dx.doi.org/10.3390/cells9040963.
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The neurotropic and extremophilic black yeast Exophiala dermatitidis (Herpotrichellaceae) inhabits diverse indoor environments, in particular bathrooms, steam baths, and dishwashers. Here, we show that the selected strain, EXF-10123, is polymorphic, can grow at 37 °C, is able to assimilate aromatic hydrocarbons (toluene, mineral oil, n-hexadecane), and shows abundant growth with selected neurotransmitters (acetylcholine, gamma-aminobutyric acid, glycine, glutamate, and dopamine) as sole carbon sources. We have for the first time demonstrated the effect of E. dermatitidis on neuroblastoma cell model SH-SY5Y. Aqueous and organic extracts of E. dermatitidis biomass reduced SH-SY5Y viability by 51% and 37%, respectively. Melanized extracellular vesicles (EVs) prepared from this strain reduced viability of the SH-SY5Y to 21%, while non-melanized EVs were considerably less neurotoxic (79% viability). We also demonstrated direct interactions of E. dermatitidis with SH-SY5Y by scanning electron and confocal fluorescence microscopy. The observed invasion and penetration of neuroblastoma cells by E. dermatitidis hyphae presumably causes the degradation of most neuroblastoma cells in only three days. This may represent a so far unknown indirect or direct cause for the development of some neurodegenerative diseases such as Alzheimer’s.
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Chen, Jian, Chuan Jiang, Juan Du, and Chun-Li Xie. "MiR-142-5p Protects Against 6-OHDA-Induced SH-SY5Y Cell Injury by Downregulating BECN1 and Autophagy." Dose-Response 18, no. 1 (January 1, 2020): 155932582090701. http://dx.doi.org/10.1177/1559325820907016.
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Background: MiR-142-5p has been demonstrated to hold significant implications in neurological diseases. However, the impact and underlying regulatory mechanism of miR-142-5p in Parkinson’s disease (PD) are still ominous. Methods: To simulate the PD, 6-hydroxydopamine (6-OHDA)-treated SH-SY5Y cell model was used in this study. Levels of messenger RNA and protein were tested by quantitative real-time polymerase chain reaction and Western blot analyses, respectively. The direct interaction between miR-142-5p and Beclin 1 (BECN1) was assessed by luciferase reporter assay. Furthermore, Cell Counting Kit-8 assay was performed to assess cytotoxicity of SH-SY5Y cell. Results: In consequence, a significant decrease of miR-142-5p was observed in 6-OHDA-induced SH-SY5Y cells. Over-/Low-expressed miR-142-5p resulted in a significant enhancement/inhibition on cell vitalities of 6-OHDA-treated SH-SY5Y cells, which might be modulated by repressing cellular autophagy through inhibiting level of BECN1 and LC3 II/LC3 I and elevating P62 level. Luciferase reporter assay showed that the BECN1 was the target gene of miR-142-5p. Additionally, the loss/gain of BECN1 rescued/blocked the effects of miR-142-5p on the viability of 6-OHDA-induced SH-SY5Y cells. Conclusions: These results highlight that miR-142-5p functions as a neuroprotective regulator in 6-OHDA-induced neuronal SH-SY5Y cells simulating PD model in vitro via regulating autophagy-related protein BECN1 and autophagy to influence cell viability.
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D., Rohini, and Vijayalakshmi K. "SESAMOL ANTAGONIZES ROTENONE-INDUCED CELL DEATH IN SH-SY5Y NEURONAL CELLS." International Journal of Pharmacy and Pharmaceutical Sciences 8, no. 12 (December 1, 2016): 72. http://dx.doi.org/10.22159/ijpps.2016v8i12.14529.
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<p><strong>Objective: </strong>To investigate the neuroprotective effect of sesamol against rotenone-induced cell death in SH-SY5Y cells associated with Parkinsonism.</p><p><strong>Methods: </strong>SH-SY5Y cells were maintained in Dulbecco’s modified Eagle’s medium. After differentiation, the cells were incubated with rotenone (20 μM) and sesamol at different concentrations (10-100 μM). Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. The reactive oxygen species, mitochondrial membrane potential and nuclear morphology were determined by dichlorofluorescein diacetate, rhodamine 123 and 4’, 6-diamidino-2-phenylindole, respectively. Thiobarbituric acid reactive substances, activities of catalase, superoxide dismutase, and glutathione peroxidase and glutathione level were determined by standard assays.</p><p><strong>Results: </strong>Sesamol significantly increased the cell viability and decreased the rotenone-induced cell death in SH-SY5Y cells. Sesamol antagonized rotenone-induced reactive oxygen species generation, loss of mitochondrial membrane potential and nuclear damage. Sesamol also decreased thiobarbituric acid reactive substances level, increased the activities of catalase, superoxide dismutase, glutathione peroxidase and increased the level of glutathione in rotenone-induced cells.</p><p><strong>Conclusion: </strong>The results obtained strongly indicate the promising neuroprotective role of sesamol against rotenone-induced death in SH-SY5Y cells.</p>
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Shih, Yu-Tzu, Ing-Jun Chen, Yang-Chang Wu, and Yi-Ching Lo. "San-Huang-Xie-Xin-Tang Protects against Activated Microglia- and 6-OHDA-Induced Toxicity in Neuronal SH-SY5Y Cells." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–11. http://dx.doi.org/10.1093/ecam/nep025.
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San-Huang-Xie-Xin-Tang (SHXT), composed ofCoptidis rhizoma,Scutellariae radixandRhei rhizoma, is a traditional Chinese herbal medicine used to treat gastritis, gastric bleeding and peptic ulcers. This study investigated the neuroprotective effects of SHXT on microglia-mediated neurotoxicity using co-cultured lipopolysaccharide (LPS)-activated microglia-like BV-2 cells with neuroblastoma SH-SY5Y cells. Effects of SHXT on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity were also examined in SH-SY5Y cells. Results indicated SHXT inhibited LPS-induced inflammation of BV-2 cells by downregulation of iNOS, NO, COX-2, PGE2, gp91phox, iROS, TNF-α, IL-1β, inhibition of IκBα degradation and upregulation of HO-1. In addition, SHXT increased cell viability and down regulated nNOS, COX-2 and gp91phoxof SH-SY5Y cells co-cultured with LPS activated BV-2 cells. SHXT treatment increased cell viability and mitochondria membrane potential (MMP), decreased expression of nNOS, COX-2, gp91phoxand iROS, and inhibited IκBα degradation in 6-OHDA-treated SH-SY5Y cells. SHXT also attenuated LPS activated BV-2 cells- and 6-OHDA-induced cell death in differentiated SH-SY5Y cells with db-cAMP. Furthermore, SHXT-inhibited nuclear translocation of p65 subunit of NF-κB in LPS treated BV-2 cells and 6-OHDA treated SH-SY5Y cells. In conclusion, SHXT showed protection from activated microglia- and 6-OHDA-induced neurotoxicity by attenuating inflammation and oxidative stress.
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Zhu, Li, Ning Ning, Yu Li, Qiu-Fang Zhang, Yong-Chao Xie, Maida Irshad, Xing Feng, and Xiao-Jun Tao. "Biatractylolide Modulates PI3K-Akt-GSK3β-Dependent Pathways to Protect against Glutamate-Induced Cell Damage in PC12 and SH-SY5Y Cells." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/1291458.
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Biatractylolide, isolated from the ethyl acetate extract of Atractylodes macrocephala, has shown various pharmacological activities such as antitumor and antioxidant activities. In this work, we aim to study the protective effect of biatractylolide on glutamate-induced rat adrenal pheochromocytoma cell (PC12) and human bone marrow neuroblastoma cell line (SH-SY5Y) injury and preliminarily explore its mechanism. The results showed that glutamate was cytotoxic with an inhibitory concentration 50% (IC50) of 8.5 mM in PC12 and 10 mM in SH-SY5Y cells. In this work, the preincubation with biatractylolide (10, 15, and 20 μM) observably improved cell viability, inhibited the apoptosis of cells induced by glutamate, and reduced the activity of LDH. AO staining revealed that apoptosis of cells was decreased. Additionally, the results of western blotting manifested that pretreatment with biatractylolide could downregulate GSK3β protein expression and upregulate p-Akt protein expression, thereby protecting PC12 and SH-SY5Y cells from injury. All these findings indicate that biatractylolide has a neuroprotective effect on glutamate-induced injury in PC12 and SH-SY5Y cells through a mechanism of the PI3K-Akt-GSK3β-dependent pathways.
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Nishtuk, Y. V., O. V. Stasyk, and O. G. Stasyk. "Spermidine activates authophagy but does not rescue human neuroblastoma SH-SY5Y cells from effects of arginine starvation." Studia Biologica 16, no. 3 (October 4, 2022): 35–48. http://dx.doi.org/10.30970/sbi.1603.691.
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Background. Neuroblastoma is a malignant tumor of the sympathetic nervous system common in early childhood. Autophagy is manifested in neuroblastoma cells at basal levels, but is often upregulated in cells of the aggressive neuroblastoma forms. The aim of the study was to evaluate effects of polyamine spermidine and deficiency of arginine on cell viability and autophagy regulation in cells of human neuroblastoma. Materials and Methods. The human neuroblastoma SH-SY5Y cell line was an experimental model for the MTT assay of metabolic activity and cell viability upon exposure to different concentrations of spermidine in complete and arginine-free media. Assessing autophagy induction under arginine deficiency and spermidine treatment was carried out using fluorescence microscopy of neuroblastoma cells labeled with autophagic lysosomes-staining dye monodancylcadaverine. Results and Discussion. It was found that arginine withdrawal abrogates proliferation of SH-SY5Y cells. In the presence of arginine precursor, citrulline, in arginine-free medium, SH-SY5Y cells could not proliferate and, therefore, are auxotrophic for arginine. SH-SY5Y cells were more sensitive to arginine starvation than to starvation for indispensible amino acids lysine or leucine. It was also revealed that spermidine at low concentrations of 5-10 μM did not affect SH-SY5Y cells viability irrespective of arginine availability. However, at 50 and higher concentrations this polyamine was highly cytotoxic in arginine-sufficient or deficient media. Analysis of autophagy induction by spermidine and under arginine starvation revealed an increase in the number of autophagic lysosomes in SH-SY5Y cells and additive effect of the two stimuli. Conclusion. The described experiments revealed that arginine deprivation abrogated proliferation, led to a decrease in cell viability and induced autophagy in human neuroblastoma SH-SY5Y cells. Spermidine at the concentrations of 5-10 μM, while upinducing autophagy, did not improve survival of SH-SY5Y cells under arginine deprivation, whereas at a concentration above 50 μM spermidine had a strong cytotoxic effect. The main observation of this study is that autophagy can be readily manipulated in neuroblastoma cells by simultaneous deprivation for arginine and spermidine treatment.
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Zapatero-Belinchón, Francisco, Erik Dietzel, Olga Dolnik, Katinka Döhner, Rui Costa, Barbara Hertel, Barbora Veselkova, et al. "Characterization of the Filovirus-Resistant Cell Line SH-SY5Y Reveals Redundant Role of Cell Surface Entry Factors." Viruses 11, no. 3 (March 19, 2019): 275. http://dx.doi.org/10.3390/v11030275.
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Filoviruses infect a wide range of cell types with the exception of lymphocytes. The intracellular proteins cathepsin B and L, two-pore channel 1 and 2, and bona fide receptor Niemann–Pick Disease C1 (NPC1) are essential for the endosomal phase of cell entry. However, earlier steps of filoviral infection remain poorly characterized. Numerous plasma membrane proteins have been implicated in attachment but it is still unclear which ones are sufficient for productive entry. To define a minimal set of host factors required for filoviral glycoprotein-driven cell entry, we screened twelve cell lines and identified the nonlymphocytic cell line SH-SY5Y to be specifically resistant to filovirus infection. Heterokaryons of SH-SY5Y cells fused to susceptible cells were susceptible to filoviruses, indicating that SH-SY5Y cells do not express a restriction factor but lack an enabling factor critical for filovirus entry. However, all tested cell lines expressed functional intracellular factors. Global gene expression profiling of known cell surface entry factors and protein expression levels of analyzed attachment factors did not reveal any correlation between susceptibility and expression of a specific host factor. Using binding assays with recombinant filovirus glycoprotein, we identified cell attachment as the step impaired in filovirus entry in SH-SY5Y cells. Individual overexpression of attachment factors T-cell immunoglobulin and mucin domain 1 (TIM-1), Axl, Mer, or dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) rendered SH-SY5Y cells susceptible to filovirus glycoprotein-driven transduction. Our study reveals that a lack of attachment factors limits filovirus entry and provides direct experimental support for a model of filoviral cell attachment where host factor usage at the cell surface is highly promiscuous.
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Gangras, Pooja, Valentina Gelfanova, Graham D. Williams, Samuel K. Handelman, Ryan M. Smith, and Marjoke F. Debets. "Investigating SH-SY5Y Neuroblastoma Cell Surfaceome as a Model for Neuronal-Targeted Novel Therapeutic Modalities." International Journal of Molecular Sciences 23, no. 23 (December 1, 2022): 15062. http://dx.doi.org/10.3390/ijms232315062.
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The SH-SY5Y neuroblastoma cells are a widely used in vitro model approximating neurons for testing the target engagement of therapeutics designed for neurodegenerative diseases and pain disorders. However, their potential as a model for receptor-mediated delivery and uptake of novel modalities, such as antibody-drug conjugates, remains understudied. Investigation of the SH-SY5Y cell surfaceome will aid in greater in vitro to in vivo correlation of delivery and uptake, thereby accelerating drug discovery. So far, the majority of studies have focused on total cell proteomics from undifferentiated and differentiated SH-SY5Y cells. While some studies have investigated the expression of specific proteins in neuroblastoma tissue, a global approach for comparison of neuroblastoma cell surfaceome to the brain and dorsal root ganglion (DRG) neurons remains uninvestigated. Furthermore, an isoform-specific evaluation of cell surface proteins expressed on neuroblastoma cells remains unexplored. In this study, we define a bioinformatic workflow for the identification of high-confidence surface proteins expressed on brain and DRG neurons using tissue proteomic and transcriptomic data. We then delineate the SH-SY5Y cell surfaceome by surface proteomics and show that it significantly overlaps with the human brain and DRG neuronal surface proteome. We find that, for 32% of common surface proteins, SH-SY5Y-specific major isoforms are alternatively spliced, maintaining their protein-coding ability, and are predicted to localize to the cell surface. Validation of these isoforms using surface proteomics confirms a SH-SY5Y-specific alternative NRCAM (neuron-glia related cell adhesion molecule) isoform, which is absent in typical brain neurons, but present in neuroblastomas, making it a receptor of interest for neuroblastoma-specific therapeutics.
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ZHAO, SHIJIA, ALEX STAMM, JEONG SOON LEE, ALEXEI GRUVERMAN, JUNG YUL LIM, and LINXIA GU. "ELASTICITY OF DIFFERENTIATED AND UNDIFFERENTIATED HUMAN NEUROBLASTOMA CELLS CHARACTERIZED BY ATOMIC FORCE MICROSCOPY." Journal of Mechanics in Medicine and Biology 15, no. 05 (October 2015): 1550069. http://dx.doi.org/10.1142/s0219519415500694.
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Human neuroblastoma (SH-SY5Y) cells, with its ability to differentiate into neurons, have been widely used as the in vitro cell culture model for neuroscience research, especially in studying the pathogenesis of Parkinson's disease (PD) and developing therapeutic strategies. Cellular elasticity could potentially serve as a biomarker to quantitatively distinguish undifferentiated and differentiated SH-SY5Y cells. The goal of this work is to characterize the retinoic acid (RA) induced alternations of elastic properties of SH-SY5Y cells using atomic force microscopy (AFM). The elasticity was measured at multiple points of a single cell. Results have shown that the differentiation of SH-SY5Y cell led to a larger elastic modulus, which is three times more than that of undifferentiated cells. A higher indentation rate applied during AFM measurements led to a larger elastic modulus of the cell. This work provides new insights into the differentiation process identified by the elasticity marker, which could be extended to investigate the function, health and ageing of cells.
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Alarifi, Saud, Daoud Ali, and Saad Alkahtani. "Oxidative Stress-Induced DNA Damage by Manganese Dioxide Nanoparticles in Human Neuronal Cells." BioMed Research International 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/5478790.
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Metal nanoparticles have been extensively used in industry as well as in biomedical application. In this work, we have evaluated the toxic potential of manganese dioxide (MnO2) nanoparticles (MNPs) on human neuronal (SH-SY5Y) cells. Cellular toxicity due to MNPs (0, 10, 30, and 60 μg/ml) on the SH-SY5Y cell was observed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and neutral red uptake (NRU) tests. MNPs produced reactive oxygen species (ROS) and declined in mitochondrial membrane potential in the SH-SY5Y cell in dose and duration dependent manner. Moreover, lipid peroxide (LPO), superoxide dismutase (SOD), and catalase (CAT) activities were increased and glutathione was reduced in dose and time dependent manner. A significant upgrade in Hoechst 33342 fluorescence intensity (chromosome condensation) and phosphatidylserine translocation (apoptotic cell) was visualized in cells treated with MNPs for 48 h. On the other hand, caspase-3 activity was increased due to MNPs in SH-SY5Y cells. DNA strand breaks were determined by alkaline single cell gel electrophoresis assay (Comet Assay) and maximum fragmentation of DNA produced due to MNPs (60 μg/ml) for 48 hours. This result provides a basic mechanism of induction of apoptosis and toxicity by MNPs in SH-SY5Y cells.
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Zhang, Zhen-Dong, Ya-Jun Yang, Zhe Qin, Xi-Wang Liu, Shi-Hong Li, Li-Xia Bai, and Jian-Yong Li. "Protective Activity of Aspirin Eugenol Ester on Paraquat-Induced Cell Damage in SH-SY5Y Cells." Oxidative Medicine and Cellular Longevity 2021 (August 4, 2021): 1–17. http://dx.doi.org/10.1155/2021/6697872.
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Aspirin eugenol ester (AEE) is a new pharmaceutical compound esterified by aspirin and eugenol, which has anti-inflammatory, antioxidant, and other pharmacological activities. The aim of this study was to investigate the protective effect of AEE on paraquat- (PQ-) induced cell damage of SH-SY5Y human neuroblastoma cells and its potential molecular mechanism. There was no significant change in cell viability when AEE was used alone. PQ treatment reduced cell viability in a concentration-dependent manner. However, AEE reduced the PQ-induced loss of cell viability. Flow cytometry, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and 4 ′ 6-diamidino-2-phenylindole (DAPI) staining were used to evaluate cell apoptosis. Compared with the PQ group, AEE pretreatment could significantly inhibit PQ-induced cell damage. AEE pretreatment could reduce the cell damage of SH-SY5Y cells induced by PQ via reducing superoxide anion, intracellular reactive oxygen species (ROS), and mitochondrial ROS (mtROS) and increasing the levels of mitochondrial membrane potential ( Δ Ψ m ). At the same time, AEE could increase the activity of glutathione peroxidase (GSH-Px), catalase (CAT), and superoxide dismutase (SOD) and decrease the activity of malondialdehyde (MDA). The results showed that compared with the control group, the expression of p-PI3K, p-Akt, and Bcl-2 was significantly decreased, while the expression of caspase-3 and Bax was significantly increased in the PQ group. In the AEE group, AEE pretreatment could upregulate the expression of p-PI3K, p-Akt, and Bcl-2 and downregulate the expression of caspase-3 and Bax in SH-SY5Y cells. PI3K inhibitor LY294002 and the silencing of PI3K by shRNA could weaken the protective effect of AEE on PQ-induced SH-SY5Y cells. Therefore, AEE has a protective effect on PQ-induced SH-SY5Y cells by regulating the PI3K/Akt signal pathway to inhibit oxidative stress.
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Karademir, Mustafa, and Merve Ergül. "Esomeprazole and pantoprazole enhance the antiproliferative effects of cisplatin on the human neuroblastoma SH-SY5Y cell line." International Journal of Research in Medical Sciences 7, no. 3 (February 27, 2019): 734. http://dx.doi.org/10.18203/2320-6012.ijrms20190486.
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Background: Proton pump inhibitors (PPIs) largely used a drug to treat gastroesophageal disease such as gastric ulcers. Moreover, in recent years, several studies suggest that PPIs have an important anti-cancer effect in monotherapy and or combination with chemotherapy. The aim of this study was to investigate whether esomeprazole and pantoprazole exhibit anti-cancer effect alone or could enhance chemosensitivity on the human neuroblastoma cell line SH-SY5Y to cisplatin.Methods: The human neuroblastoma SH-SY5Y cells were cultured and treated with different concentrations of esomeprazole, pantoprazole, and cisplatin alone. Also, these cells exposed to cisplatin+ esomeprazole and cisplatin + pantoprazole combinations, respectively and incubated 24 h. The antiproliferative activities of the (PPIs) alone or in a combination of cisplatin was evaluated using the XTT colorimetric assay.Results: According to experimental data, neither PPIs showed no cytotoxicity on the human neuroblastoma cell line SH-SY5Y at all concentrations. However, when combined with cisplatin separately, they were found to have significant antiproliferative effects on the human neuroblastoma SH-SY5Y cell lines when compared to cell lines treated with cisplatin alone (p<0.05).Conclusions: Taken together, the inhibition of V-ATPase via esomeprazole and pantoprazole might enhance the chemosensitivity of cisplatin on the human neuroblastoma cell line SH-SY5Y. However, further studies are needed to be able to utilize PPIs in human neuroblastoma cells.
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Xiong, Qiu-Ju, Zhuang-Li Hu, Peng-Fei Wu, Lan Ni, Zhi-Fang Deng, Wen-Ning Wu, Jian-Guo Chen, and Fang Wang. "Acid-sensing ion channels contribute to the increase in vesicular release from SH-SY5Y cells stimulated by extracellular protons." American Journal of Physiology-Cell Physiology 303, no. 4 (August 15, 2012): C376—C384. http://dx.doi.org/10.1152/ajpcell.00067.2012.
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Acid-sensing ion channels (ASICs) have been reported to play a role in the neuronal dopamine pathway, but the exact role in neurotransmitter release remains elusive. Human neuroblastoma SH-SY5Y is a dopaminergic neuronal cell line, which can release monoamine neurotransmitters. In this study, the expression of ASICs was identified in SH-SY5Y cells to further explore the role of ASICs in vesicular release stimulated by acid. We gathered evidence that ASICs could be detected in SH-SY5Y cells. In whole cell patch-clamp recording, a rapid decrease in extracellular pH evoked inward currents, which were reversibly inhibited by 100 μM amiloride. The currents were pH dependent, with a pH of half-maximal activation (pH0.5) of 6.01 ± 0.04. Furthermore, in calcium imaging and FM 1-43 dye labeling, it was shown that extracellular protons increased intracellular calcium levels and vesicular release in SH-SY5Y cells, which was attenuated by PcTx1 and amiloride. Interestingly, N-type calcium channel blockers inhibited the vesicular release induced by acidification. In conclusion, ASICs are functionally expressed in SH-SY5Y cells and involved in vesicular release stimulated by acidification. N-type calcium channels may be involved in the increase in vesicular release induced by acid. Our results provide a preliminary study on ASICs in SH-SY5Y cells and neurotransmitter release, which helps to further investigate the relationship between ASICs and dopaminergic neurons.
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Wright, Karina T., Gareth J. Griffiths, and William E. B. Johnson. "A Comparison of High-Content Screening versus Manual Analysis to Assay the Effects of Mesenchymal Stem Cell–Conditioned Medium on Neurite Outgrowth In Vitro." Journal of Biomolecular Screening 15, no. 5 (April 16, 2010): 576–82. http://dx.doi.org/10.1177/1087057110367959.
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Bone marrow mesenchymal stem cells (MSCs) promote nerve growth and functional recovery in animal models of spinal cord injury (SCI) to varying levels. The authors have tested high-content screening to examine the effects of MSC-conditioned medium (MSC-CM) on neurite outgrowth from the human neuroblastoma cell line SH-SY5Y and from explants of chick dorsal root ganglia (DRG). These analyses were compared to previously published methods that involved hand-tracing individual neurites. Both methods demonstrated that MSC-CM promoted neurite outgrowth. Each showed the proportion of SH-SY5Y cells with neurites increased by ~200% in MSC-CM within 48 h, and the number of neurites/SH-SY5Y cells was significantly increased in MSC-CM compared with control medium. For high-content screening, the analysis was performed within minutes, testing multiple samples of MSC-CM and in each case measuring >15,000 SH-SY5Y cells. In contrast, the manual measurement of neurite outgrowth from >200 SH-SY5Y cells in a single sample of MSC-CM took at least 1 h. High-content analysis provided additional measures of increased neurite branching in MSC-CM compared with control medium. MSC-CM was also found to stimulate neurite outgrowth in DRG explants using either method. The application of the high-content analysis was less well optimized for measuring neurite outgrowth from DRG explants than from SH-SY5Y cells.
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Juntunen, Miia, Sanna Hagman, Anaick Moisan, Susanna Narkilahti, and Susanna Miettinen. "In Vitro Oxygen-Glucose Deprivation-Induced Stroke Models with Human Neuroblastoma Cell- and Induced Pluripotent Stem Cell-Derived Neurons." Stem Cells International 2020 (October 29, 2020): 1–13. http://dx.doi.org/10.1155/2020/8841026.
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Stroke is a devastating neurological disorder and one of the leading causes of mortality and disability. To understand the cellular and molecular mechanisms of stroke and to develop novel therapeutic approaches, two different in vitro human cell-based stroke models were established using oxygen-glucose deprivation (OGD) conditions. In addition, the effect of adipose stem cells (ASCs) on OGD-induced injury was studied. In the present study, SH-SY5Y human neuroblastoma cells and human induced pluripotent stem cells (hiPSCs) were differentiated into neurons, cultured under OGD conditions (1% O2) for 24 h, and subjected to a reperfusion period for 24 or 72 h. After OGD, ASCs were cocultured with neurons on inserts for 24 or 72 h to study the neuroprotective potential of ASCs. The effect of OGD and ASC coculture on the viability, apoptosis, and proliferation of and axonal damage to neuronal cells was studied. The results showed that OGD conditions induced cytotoxicity and apoptosis of SH-SY5Y- and hiPSC-derived neurons, although more severe damage was detected in SH-SY5Y-derived neurons than in hiPSC-derived neurons. Coculture with ASCs was protective for neurons, as the number of dead ASC-cocultured neurons was lower than that of control cells, and coculture increased the proliferation of both cell types. To conclude, we developed in vitro human cell-based stroke models in SH-SY5Y- and hiPSC-derived neurons. This was the first time hiPSCs were used to model stroke in vitro. Since OGD had different effects on the studied cell types, this study highlights the importance of using several cell types in in vitro studies to confirm the outcomes of the study. Here, ASCs exerted a neuroprotective effect by increasing the proliferation and decreasing the death of SH-SY5Y- and hiPSC-derived neurons after OGD.
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Li, Qianqian, Tingjiao Liu, Shanshan Yang, and Zhongling Zhang. "Upregulation of miR-34a by Inhibition of IRE1α Has Protective Effect against Aβ-Induced Injury in SH-SY5Y Cells by Targeting Caspase-2." Oxidative Medicine and Cellular Longevity 2019 (June 2, 2019): 1–10. http://dx.doi.org/10.1155/2019/2140427.
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Background. Neurotoxicity induced by the amyloid-β (Aβ) peptide is one of the most important pathological mechanisms of Alzheimer’s disease (AD). Based on accumulating evidence in AD research, both endoplasmic reticulum stress (ER stress) and alterations in the microRNA (miRNA) network contribute to the pathogenesis of the disease, making them potential therapeutic targets for AD. The present study was performed to investigate whether miR-34a and the inositol-requiring enzyme 1 (IRE1) are involved in the regulation of Aβ-induced cytotoxicity. Methods. Human neuroblastoma SH-SY5Y cells were treated with Aβ1-40. Cell viability was assessed by the MTT assay. The integrity of the plasma membrane was assessed by LDH release. The expression levels of XBP1s, IRE1α, p-IRE1α, and Caspase-2 were detected by Western blot analysis. Spliced-XBP1 mRNA and miR-34a were detected by reverse transcription- (RT-) PCR and quantitative real-time PCR, respectively. Caspase-2 activity was measured using the Caspase-2 cellular activity assay kit. The IRE1 inhibitor (STF-083010) was used to determine the role of IRE1α on miR-34a expression. SH-SY5Y cells were transfected with miR-34a mimics to assess the role of miR-34a on the activation of Caspase-2 and the viability of Aβ-exposed SH-SY5Y cells. Results. We showed that Aβ caused concentration- and duration-dependent death of SH-SY5Y cells. The expression levels of XBP1s, p-IRE1α, and Caspase-2 were increased, along with a corresponding decrease in the miR-34a levels in Aβ-exposed SH-SY5Y cells. The IRE1 inhibitor (STF-083010) upregulated the expression of miR-34a and suppressed the activation of Caspase-2, effectively alleviating the Aβ-induced death of SH-SY5Y cells. Transfection studies show that miR-34a mimics inhibit the expression of Caspase-2 and restore the viability of Aβ-exposed SH-SY5Y cells. Conclusion. Aβ peptide induced downregulation of miR-34a through the activation of IRE1α, which may induce cytotoxicity by targeting Caspase-2. Upregulation of miR-34a by inhibition of IRE1α has protective effects against Aβ-induced injury in SH-SY5Y cells.
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Yun-Liang, Xie, and Zhang Bo. "Protective Effect of Patchouli Alcohol Against SH-SY5Y Cell Injury Induced by Aβ25-35 via the Reduction of Oxidative Stress and Apoptosis." Natural Product Communications 16, no. 7 (July 2021): 1934578X2110317. http://dx.doi.org/10.1177/1934578x211031715.
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Patchouli alcohol (PA) has multiple pharmacological activities, but its protective effect against SH-SY5Y cell injury induced by Aβ25-35 has not been reported. It has been recorded that phosphatidylinositol 3-hydroxykinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway plays an important role in neuroprotection. The purpose of this study was to investigate the protective effect of PA against SH-SY5Y cell injury induced by Aβ25-35 and its underlying mechanism. The results showed that compared with that in the Aβ25-35-induced injury group, the survival rate of SH-SY5Y cells increased ( P < .01) in the different PA-treated groups and the lactic dehydrogenase activity decreased significantly ( P < .01) in the 10, 20, and 40 μg/mL PA groups; compared with those in the Aβ25-35-induced injury group, the malonyldialdehyde contents in SH-SY5Y cells decreased ( P < .05 or P < .01), while the superoxide dismutase, glutathione peroxidase, and catalase activities increased significantly ( P < .05 or P < .01) in the different PA-treated groups; compared with those in the Aβ25-35-induced injury group, the apoptosis rates, and the mRNA and protein levels of Caspase-3 and Bax in SH-SY5Y cells decreased ( P < .05 or P < .01), while the mRNA and protein levels of Bcl-2, and phosphorylated Akt (p-Akt) and phosphorylated mTOR protein levels increased significantly ( P < .05 or P < .01) in the different PA-treated groups. The above results indicate that PA can inhibit the oxidative stress and apoptosis of SH-SY5Y cells induced by Aβ25-35 by regulating the PI3K/Akt/mTOR pathway, to protect the SH-SY5Y cells from the injury induced by Aβ25-35.
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Islam, Md Ashraful, Fadlan A. Sheikh, Shelia D. Thomas, Tarek Magrabi, Tariq Alrashid, and Donald M. Miller. "Identification of a Guanine-Rich-Oligonucleotides (GRO) in the Promoter of the MYCN Gene which Inhibits Neuroblastoma Growth." International Journal of Innovative Research in Medical Science 7, no. 06 (June 20, 2022): 284–90. http://dx.doi.org/10.23958/ijirms/vol07-i06/1422.
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Neuroblastoma is the most common solid tumor of childhood malignancy. The biological properties vary from indolent to aggressive depending on how different genes play their role in transforming neural crest cells leading to spontaneous regression to an unfavorable outcome. Guanine-Rich Oligonucleotides (GRO) are being tested as a potential target for an anti-cancer drug. In this study, we have identified GROs at the promoter regions of the MYCN oncogene (MYCN-15) and it formed quadruplex in-vitro shown by circular dichroism (CD). Then three neuroblastoma cell lines were used to explore the effect of MYCN-15 on different biological properties: cellular growth, differentiation, and death. The neuroblastoma cell lines SH-SY5Y and SK-N-AS have a single copy of the MYCN gene, whereas the SK-N-BE2 cell line has multiple copies (n-Myc amplified). MYCN-15-induced cellular differentiation in both SK-N-AS and SH-SY5Y cells was followed by cell death in the SH-SY5Y cell line only. MTT [3-(4,5-dimethylthiazol-2-Yl)-2,5-diphenyltetrazolium bromide] assay revealed, that there was modest growth inhibition in both SH-SY5Y (~58%) and SK-N-BE2 (~38%) cells when treated with MYCN-15 oligonucleotide. There were no significant changes in survivin protein expression in both SK-N-AS and SH-SY5Y cells when treated with MYCN-15 oligonucleotides. Taken together, MYCN-15 can be used as an essential target oligonucleotide for treating human neuroblastoma.
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Wen, Xianjie, Zhaoxia Wu, and Shiyuan Xu. "NNC55-0396 Reduces SH-SY5Y Cell Damage Induced by Bupivacaine Hydrochloride." Journal of Experimental and Clinical Toxicology 1, no. 3 (August 31, 2020): 17–29. http://dx.doi.org/10.14302/issn.2641-7669.ject-20-3529.
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Background Local anesthetic neurotoxicity is a common complication in clinical anesthesia, which can cause permanent nerve damage in severe cases. The T-type calcium channel is an important channel for regulating the excitability of neurons. Normally, extracellular calcium ions enter the cell through the T-type calcium channel to change the excitability of neurons. When the intracellular calcium is overloaded, it can cause cell damage. Aims To investigated the roles of T-type calcium channel in the SH-SY5Y cells injury induced by the bupivacaine. Methods The SH-SY5Y cell culture model was used to observe the effect of T-type calcium channel blocker NNC55-0396 on the neurotoxicity of bupivacaine hydrochloride by MTT methold,flow cytometry, Western blotting and other methods. Results The results show that NNC55-0396 can block the T-type calcium channel of SH-SY5Y cells, improve the decrease of cell viability caused by bupivacaine hydrochloride, reduce the level of intracellular calcium ion, reduce the expression of Cleavedcaspase-3, and reduce cell apoptosis. Conclusion The above results indicate that the T-type calcium channel is involved in the SH-SY5Y cell damage caused by bupivacaine hydrochloride, and blocking the T-type calcium channel can reduce the neurotoxicity of bupivacaine hydrochloride.
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Serdar, Belgin Sert, Tuğba Erkmen, Bekir Uğur Ergür, Pınar Akan, and Semra Koçtürk. "Which Medium and Ingredients Provide Better Morphological Differentiation of SH-SY5Y Cells?" Proceedings 2, no. 25 (December 5, 2018): 1577. http://dx.doi.org/10.3390/proceedings2251577.
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Human SH-SY5Y cell line has been used as an in vitro model in neuroscience research. However, many researchers emphasized that there are many differences between differentiated and undifferentiated characteristics of SH-SY5Y. Although Retinoic Acid (RA) generally have been used for differentiation of SH-SY5Y cells, which protocol provides better differentiation have not been cleared yet. Therefore, we compared RA and the other mediums in different treatment periods for obtaining better differentiated, carrying a neuron-like phenotype (N-type) characteristics, of SH-SY5Y human cells. The cells were pre-treated with different mediums for different treatment periods and compared with both for each other and the control group. When we pre-treated the cells with RA for 5-day and followed by the Mix medium (Neurobasal, B27, db-cAMP, KCI) and BDNF, neurite length and MAP2 expression of the cells were found significantly higher than the control group. In conclusion, we showed that more than one agent (RA) is clearly necessary to reach better differentiation of SH-SY5Y cells.
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Dieter, Fabian, Carsten Esselun, and Gunter P. Eckert. "Redox Active α-Lipoic Acid Differentially Improves Mitochondrial Dysfunction in a Cellular Model of Alzheimer and Its Control Cells." International Journal of Molecular Sciences 23, no. 16 (August 16, 2022): 9186. http://dx.doi.org/10.3390/ijms23169186.
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Introduction: Alpha lipoic acid (ALA) is a sulphur-containing organic compound, derived from octanoic acid, and an important cofactor for mitochondrial respiratory enzymes. It has strong antioxidant properties that improve mitochondrial function. We investigated if ALA improves mitochondrial dysfunction in a cellular model of Alzheimer’s disease (AD). Methods: SH-SY5Y-APP695 cells were used as a model for an early stage of AD. Vector-transfected SH-SY5Y-MOCK cells served as controls. Using these cells, we investigated mitochondrial respiration (OXPHOS), mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) production, and citrate synthase activity (CS) in cells treated with ALA. Cells were treated for 24 h with different concentrations of ALA and with or without the complex I inhibitor rotenone. Results: Incubation with ALA showed a significant increase in ATP levels in both SH-SY5Y-APP695 and SH-SY5Y-MOCK cells. MMP levels were elevated in SH-SY5Y-MOCK cells, treatment with rotenone showed a reduction in MMP, which could be partly alleviated after incubation with ALA in SH-SY5Y-MOCK cells. ALA treatment showed significant differences in respiration chain complex activities in SH-SY5Y-MOCK cells. Citrate synthase activity was unaffected. ROS levels were significantly lower in both cell lines treated with ALA. Conclusions: ALA increased the activity of the different complexes of the respiratory chain, and consequently enhanced the MMP, leading to increased ATP levels indicating improved mitochondrial function. ALA only marginally protects from additional rotenone-induced mitochondrial stress.
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Meyerson, G., K. H. Pfenninger, and S. Pahlman. "A complex consisting of pp60c-src/pp60c-srcN and a 38 kDa protein is highly enriched in growth cones from differentiated SH-SY5Y neuroblastoma cells." Journal of Cell Science 103, no. 1 (September 1, 1992): 233–43. http://dx.doi.org/10.1242/jcs.103.1.233.
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Nerve growth cones of primary neurons are highly enriched in the proto-oncogene product pp60c-src. In order to investigate this molecule further in growing neuronal cells, growth cone and cell body fractions were prepared from human SH-SY5Y neuroblastoma cells differentiated neuronally in vitro under the influence of phorbol ester. The fractions were characterized ultrastructurally and by biochemical criteria. The neuronal (pp60c-srcN) and the fibroblastic (pp60c-src) forms of pp60src are slightly enriched and activated in the growth cones relative to the perikarya. Immunoprecipitates of pp60src from differentiated SH-SY5Y growth cones contain at least four phosphoproteins in addition to pp60src. One of these, pp38, migrates as a 100–140 kDa complex with pp60src under non-reducing conditions of gel electrophoresis. The pp38/pp60src complex is not easily detected in non-differentiated SH-SY5Y cells or perikarya of differentiated SH-SY5Y cells, but it is highly enriched in the growth cone preparation. These data suggest that growth-cone pp60src exists in a disulfide-linked oligomeric complex. The complex appears to be assembled only in the cell periphery and may be dependent upon neuronal differentiation.
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Yang, Ming-Hui, Ko-Chin Chen, Pei-Wen Chiang, Tze-Wen Chung, Wan-Jou Chen, Pei-Yu Chu, Sharon Chia-Ju Chen, et al. "Proteomic Profiling of Neuroblastoma Cells Adhesion on Hyaluronic Acid-Based Surface for Neural Tissue Engineering." BioMed Research International 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/1917394.
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The microenvironment of neuron cells plays a crucial role in regulating neural development and regeneration. Hyaluronic acid (HA) biomaterial has been applied in a wide range of medical and biological fields and plays important roles in neural regeneration. PC12 cells have been reported to be capable of endogenous NGF synthesis and secretion. The purpose of this research was to assess the effect of HA biomaterial combining with PC12 cells conditioned media (PC12 CM) in neural regeneration. Using SH-SY5Y cells as an experimental model, we found that supporting with PC12 CM enhanced HA function in SH-SY5Y cell proliferation and adhesion. Through RP-nano-UPLC-ESI-MS/MS analyses, we identified increased expression of HSP60 and RanBP2 in SH-SY5Y cells grown on HA-modified surface with cotreatment of PC12 CM. Moreover, we also identified factors that were secreted from PC12 cells and may promote SH-SY5Y cell proliferation and adhesion. Here, we proposed a biomaterial surface enriched with neurotrophic factors for nerve regeneration application.
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Xiu, Mingyu, Hengfei Luan, Xiaojiao Gu, Chuang Liu, and Deming Xu. "MicroRNA-17-5p Protects against Propofol Anesthesia-Induced Neurotoxicity and Autophagy Impairment via Targeting BCL2L11." Computational and Mathematical Methods in Medicine 2022 (June 28, 2022): 1–11. http://dx.doi.org/10.1155/2022/6018037.
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Background. Propofol (PPF) has been shown in studies to cause cognitive impairment and neuronal cell death in developing animals. PPF has been demonstrated to decrease the expression of microRNA-17-5p (miR-17-5p) in a recent study. Nonetheless, the function of miR-17-5p in PPF-induced neurotoxicity and related mechanisms is uncharacterized. Methods. After the induction of neurotoxicity by treating the SH-SY5Y cells with PPF, qRT-PCR was conducted to evaluate the level of miR-17-5p. Using MTT and flow cytometry, cell viability and apoptosis rate were assessed, respectively. Interaction between miR-17-5p and BCL2 like 11 was (BCL2L11) studied using a Luciferase reporter assay. With the help of western blot analysis, we determined the level of proteins of apoptosis-related genes and autophagy-related markers. Results. In SH-SY5Y cells, PPF treatment induced neurotoxicity and downregulated miR-17-5p expression. In SH-SY5Y cells post-PPF exposure, overexpression of miR-17-5p increased cell viability and decreased apoptosis. Consistently, miR-17-5p mimics mitigated PPF-generated autophagy via inhibition of Atg5, Beclin1, and LC3II/I level and elevation of p62 protein expression. In addition, BCL2L11, which was highly expressed in PPF-treated SH-SY5Y cells, was directly targeted by miR-17-5p. Further, in PPF-treated SH-SY5Y cells, overexpressed BCL2L11 counteracted the suppressing behavior of miR-17-5p elevation on PPF-induced apoptosis. Conclusion. Overexpressed miR-17-5p alleviates PPF exposure-induced neurotoxicity and autophagy in SH-SY5Y cells via binding to BCL2L11, suggesting the possibility that miR-17-5p can serve as a candidate in the treatment of neurotoxicity (caused by PPF).
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Pandur, Edina, Edit Varga, Kitti Tamási, Ramóna Pap, Judit Nagy, and Katalin Sipos. "Effect of Inflammatory Mediators Lipopolysaccharide and Lipoteichoic Acid on Iron Metabolism of Differentiated SH-SY5Y Cells Alters in the Presence of BV-2 Microglia." International Journal of Molecular Sciences 20, no. 1 (December 20, 2018): 17. http://dx.doi.org/10.3390/ijms20010017.
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Lipopolysaccharide (LPS) and lipoteichoic acid (LTA), the Gram-negative and the Gram-positive bacterial cell wall components are important mediators of neuroinflammation in sepsis. LPS and LTA are potent activators of microglial cells which induce the production of various pro-inflammatory cytokines. It has been demonstrated that disturbance of iron homeostasis of the brain is one of the underlying causes of neuronal cell death but the mechanisms contributing to this process are still questionable. In the present study, we established monocultures of differentiated SH-SY5Y cells and co-cultures of differentiated SH-SY5Y cells and BV-2 microglia as neuronal model systems to selectively examine the effect of inflammatory mediators LPS and LTA on iron homeostasis of SH-SY5Y cells both in mono- and co-cultures. We monitored the IL-6 and TNFα secretions of the treated cells and determined the mRNA and protein levels of iron importers (transferrin receptor-1 and divalent metal transporter-1), and iron storing genes (ferritin heavy chain and mitochondrial ferritin). Moreover, we examined the relation between hepcidin secretion and intracellular iron content. Our data revealed that LPS and LTA triggered distinct responses in SH-SY5Y cells by differently changing the expressions of iron uptake, as well as cytosolic and mitochondrial iron storage proteins. Moreover, they increased the total iron contents of the cells but at different rates. The presence of BV-2 microglial cells influenced the reactions of SH-SY5Y cells on both LPS and LTA treatments: iron uptake and iron storage, as well as the neuronal cytokine production have been modulated. Our results demonstrate that BV-2 cells alter the iron metabolism of SH-SY5Y cells, they contribute to the iron accumulation of SH-SY5Y cells by manipulating the effects of LTA and LPS proving that microglia are important regulators of neuronal iron metabolism at neuroinflammation.
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Chetsawang, Jirapa, Piyarat Govitrapong, and Banthit Chetsawang. "Hydrogen Peroxide Toxicity Induces Ras Signaling in Human Neuroblastoma SH-SY5Y Cultured Cells." Journal of Biomedicine and Biotechnology 2010 (2010): 1–4. http://dx.doi.org/10.1155/2010/803815.
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It has been reported that overproduction of reactive oxygen species occurs after brain injury and mediates neuronal cells degeneration. In the present study, we examined the role of Ras signaling on hydrogen peroxide-induced neuronal cells degeneration in dopaminergic neuroblastoma SH-SY5Y cells. Hydrogen peroxide significantly reduced cell viability in SH-SY5Y cultured cells. An inhibitor of the enzyme that catalyzes the farnesylation of Ras proteins, FTI-277, and a competitive inhibitor of GTP-binding proteins, GDP-beta-S significantly decreased hydrogen peroxide-induced reduction in cell viability in SH-SY5Y cultured cells. The results of this study might indicate that a Ras-dependent signaling pathway plays a role in hydrogen peroxide-induced toxicity in neuronal cells.
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Phitthayaphong, Phansa, Sirinart Kumfu, Nipon Chattipakorn, and Siriporn C. Chattipakorn. "Blockage of Fc Gamma Receptors Alleviates Neuronal and Microglial Toxicity Induced by Palmitic Acid." Journal of Alzheimer's Disease 82, no. 3 (August 3, 2021): 1315–32. http://dx.doi.org/10.3233/jad-210417.
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Background: Palmitic acid (PA) promotes brain pathologies including Alzheimer’s disease (AD)-related proteins, neuroinflammation, and microglial activation. The activation of neurons and microglia via their Fc gamma receptors (FcγRs) results in producing inflammatory cytokines. Objective: To investigate the expression of FcγRs, FcγR signaling proteins, AD-related proteins, proinflammatory cytokines, and cell viability of neurons and microglia in association with PA exposure as well as the effects of FcγR blockade on these parameters in response to PA. Methods: 200 and 400μM PA-conjugated BSA were applied to SH-SY5Y and HMC3 cells for 24 h. For FcγR blockage experiment, both cells were exposed to FcγR blocker before receiving of 200 and 400μM of PA-conjugated BSA for 24 h. Results: PA significantly increased AD-related proteins, including Aβ and BACE1, as well as increasing TNFα, IL-1β, and IL-6 in SH-SY5Y and HMC3 cells. However, the p-Tau/Tau ratio was only increased in SH-SY5Y cells. These results were associated with an increase in FcγRs activation and a decrease in cell viability in both cell types. FcγRs blockage diminished the activation of FcγR in SH-SY5Y and HMC3 cells. Interestingly, blocking FcγRs before PA exposure reduced the increment of AD-related proteins, proinflammatory cytokines caused by PA. FcγRs blocking also inhibits cell death for 23%of SH-SY5Y cells and 64%of HMC3 cells, respectively. Conclusion: These findings suggest that PA is a risk factor for AD via the increased AD-related pathologies, inflammation, FcγRs activation, and brain cell death, while FcγR blockage can alleviate these effects.
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Wang, Liling, Jianhua Mi, Yeping Song, and Pengfei Wang. "Protective effect of EGb761 against Aβ1-42 -induced SHSY5Y cells injury and blood-brain barrier disruption via regulating Akt/Nrf2 signaling pathway." Tropical Journal of Pharmaceutical Research 20, no. 9 (November 7, 2021): 1811–18. http://dx.doi.org/10.4314/tjpr.v20i9.5.
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Purpose: Alzheimer’s disease (AD) is a common disease in the world caused by deposition in the brain parenchyma, accumulation of beta amyloid which leads to the blood brain barrier (BBB) disruption. Regardless of enough progress in the treatment of AD, the principal mechanism of BBB injury is yet not clear.Methods: In this study we examined the impact of EGb761on Aβ 1-42-induced SH-SY5Y cells in vitro model of AD. Cell viability was assessed by using MTT assay, flow cytometry was used to check the rate of cell apoptosis, ROS generation and BBB leakage was assessed by measuring the level of fluorescence in Aβ-induced SH-SY5Y cells using a reactive oxygen species kit assay and BBB permeability assay, and mRNA levels of Bax, Bcl-2, caspase-3 was measured by using RT-qPCR. Furthermore, western blot analysis was used to measure the protein expressions of Akt, Nrf2 and HO-1 in Aβ 1-42-induced SH-SY5Y cells.Results: The effect of EGb761 was investigated on the cell apoptosis induced by Aβ 1-42 andgeneration of ROS and we found that EGb761 plays a protective role against cell injury induced by Aβ 1-42. Cell apoptosis and ROS generation in SH-SY5Y cells decreased significantly with the treatment of EGb761. Furthermore, BBB permeability reduced considerably when the cells treated with EGb761 and the expression levels of Caspase-3 and Bax decreased while that of Bcl-2 were markedly increased in the Aβ 1-42-induced SH-SY5Y cells. Also, an increased in expression levels of p-Akt, Nrf2 (nucleus) and HO-1 was observed with the treatment of EGb761 in Aβ 1-42-induced SH-SY5Y cells.Conclusion: It can be concluded from these results that EGb761 could play a protective role byinhibiting apoptosis and protect Aβ 1-42-induced cell injury in vitro model of AD via activating Akt/Nrf2signaling pathway. Our study suggested that EGb761 might be a therapeutic agent for the preventionand treatment of AD.
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Valek, Lucie, and Irmgard Tegeder. "Nucleoredoxin Knockdown in SH-SY5Y Cells Promotes Cell Renewal." Antioxidants 10, no. 3 (March 13, 2021): 449. http://dx.doi.org/10.3390/antiox10030449.
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Nucleoredoxin (NXN) is a redox regulator of Disheveled and thereby of WNT signaling. Deficiency in mice leads to cranial dysmorphisms and defects of heart, brain, and bone, suggesting defects of cell fate determination. We used shRNA-mediated knockdown of NXN in SH-SY5Y neuroblastoma cells to study its impact on neuronal cells. We expected that shNXN cells would easily succumb to redox stress, but there were no differences in viability on stimulation with hydrogen peroxide. Instead, the proliferation of naïve shNXN cells was increased with a higher rate of mitotic cells in cell cycle analyses. In addition, basal respiratory rates were higher, whereas the relative change in oxygen consumption upon mitochondrial stressors was similar to control cells. shNXN cells had an increased expression of redox-sensitive heat shock proteins, Hsc70/HSPA8 and HSP90, and autophagy markers suggested an increase in autophagosome formation upon stimulation with bafilomycin and higher flux under low dose rapamycin. A high rate of self-renewal, autophagy, and upregulation of redox-sensitive chaperones appears to be an attractive anti-aging combination if it were to occur in neurons in vivo for which SH-SY5Y cells are a model.
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Mattsson, M. E., G. Enberg, A. I. Ruusala, K. Hall, and S. Påhlman. "Mitogenic response of human SH-SY5Y neuroblastoma cells to insulin-like growth factor I and II is dependent on the stage of differentiation." Journal of Cell Biology 102, no. 5 (May 1, 1986): 1949–54. http://dx.doi.org/10.1083/jcb.102.5.1949.
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Human insulin-like growth factor I and II (IGF-I and IGF-II) in concentrations of 1-30 ng/ml, were shown to stimulate ornithine decarboxylase activity and [3H]thymidine incorporation in human SH-SY5Y neuroblastoma cells. Proliferation of these cells was also stimulated by IGF-I and II when added to RPMI 1640 medium, fortified with selenium, hydrocortisone, transferrin, and beta-estradiol. Labeled IGF-I and II bound to SH-SY5Y cells. The cross-reaction pattern of IGF-I, IGF-II, and insulin in competing with the binding of labeled IGF-I and IGF-II, respectively, indicated that SH-SY5Y cells express both type I and type II IGF receptors. Treatment of SH-SY5Y cells for 4 d with 12-O-tetradecanoylphorbol-13-acetate (TPA), which resulted in morphological and functional differentiation and growth inhibition, abolished the mitogenic response to both IGF-I and II. Concomitantly, the binding of IGF-II disappeared almost totally, which offers a possible explanation for the reduced biological response to IGF-II after TPA treatment. In contrast, the IGF-I binding in TPA-treated cells was only reduced to approximately 70% of the binding to control cells. It is therefore not excluded that the IGF-I receptor could be uncoupled by TPA, with persistent binding capacity for IGF-I.
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Riegerová, Petra, Jindřich Brejcha, Dagmar Bezděková, Tomáš Chum, Eva Mašínová, Nikola Čermáková, Saak V. Ovsepian, Marek Cebecauer, and Martin Štefl. "Expression and Localization of AβPP in SH-SY5Y Cells Depends on Differentiation State." Journal of Alzheimer's Disease 82, no. 2 (July 21, 2021): 485–91. http://dx.doi.org/10.3233/jad-201409.
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Neuroblastoma cell line SH-SY5Y, due to its capacity to differentiate into neurons, easy handling, and low cost, is a common experimental model to study molecular events leading to Alzheimer’s disease (AD). However, it is prevalently used in its undifferentiated state, which does not resemble neurons affected by the disease. Here, we show that the expression and localization of amyloid-β protein precursor (AβPP), one of the key molecules involved in AD pathogenesis, is dramatically altered in SH-SY5Y cells fully differentiated by combined treatment with retinoic acid and BDNF. We show that insufficient differentiation of SH-SY5Y cells results in AβPP mislocalization.
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Dong, L. i., Yumin Zheng, Lianbo Gao, and Xiaoguang Luo. "lncRNA NEAT1 prompts autophagy and apoptosis in MPTP-induced Parkinson’s disease by impairing miR-374c-5p." Acta Biochimica et Biophysica Sinica 53, no. 7 (May 14, 2021): 870–82. http://dx.doi.org/10.1093/abbs/gmab055.
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Abstract Long non-coding RNAs (lncRNAs) play biological roles in brain disorder and neurodegenerative diseases. As the functions of lncRNA NEAT1 in Parkinson’s disease (PD) remain unknown, in the present study, we aimed to explore the roles and underlying molecular mechanisms of NEAT1 in PD. A PD mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and a cell model of SH-SY5Y induced by N-methyl-4-phenylpyridinium (MPP+) were established. The ratio of tyrosine hydroxylase (TH+) cells was determined by immunofluorescence assay, and the behavioral changes in mice were observed using pole tests and rotarod tests. The cellular viability and apoptosis of SH-SY5Y were detected by MTT assay and flow cytometric analysis, respectively, and the number of autophagosomes was subsequently measured by transmission electron microscopy. High-performance liquid chromatography was performed to detect the content of dopamine, and a dual-luciferase reporter assay was used to clarify the target of NEAT1 simultaneously. The results demonstrated that the level of NEAT1 was upregulated in the MPTP-induced PD mice, dopamine neurons, and the SH-SY5Y cells treated with MPP+, whereas the level of miR-374c-5p was downregulated. NEAT1 level was positively correlated with MPP+ in a concentration-dependent manner. NEAT1 inhibition efficiently facilitated cell proliferation but inhibited apoptosis and autophagy in the MPP+-treated SH-SY5Y cells. Additionally, silencing of NEAT1 increased the TH+ rate of neurons and suppressed autophagy greatly in PD mice. As a possible target of NEAT1, miR-374c-5p could impact on the apoptosis and autophagy of the SH-SY5Y cells. NEAT1 inhibition upregulated the expression of miR-374c-5p, enhanced SH-SY5Y cell viability, and repressed autophagy and apoptosis in MPTP-induced PD mice. These findings indicated a potential therapeutic role of NEAT1 in treating PD.
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Forster, J. I., S. Köglsberger, C. Trefois, O. Boyd, A. S. Baumuratov, L. Buck, R. Balling, and P. M. A. Antony. "Characterization of Differentiated SH-SY5Y as Neuronal Screening Model Reveals Increased Oxidative Vulnerability." Journal of Biomolecular Screening 21, no. 5 (January 6, 2016): 496–509. http://dx.doi.org/10.1177/1087057115625190.
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The immortalized and proliferative cell line SH-SY5Y is one of the most commonly used cell lines in neuroscience and neuroblastoma research. However, undifferentiated SH-SY5Y cells share few properties with mature neurons. In this study, we present an optimized neuronal differentiation protocol for SH-SY5Y that requires only two work steps and 6 days. After differentiation, the cells present increased levels of ATP and plasma membrane activity but reduced expression of energetic stress response genes. Differentiation results in reduced mitochondrial membrane potential and decreased robustness toward perturbations with 6-hydroxydopamine. We are convinced that the presented differentiation method will leverage genetic and chemical high-throughput screening projects targeting pathways that are involved in the selective vulnerability of neurons with high energetic stress levels.
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Mat Zain, Mazatulikhma Mat Zain, Nursyamila Shamsuddin, and Mohd Shihabuddin Ahmad Noorden. "The The Effects of Centella asiatica Extract (CAE) on Methamphetamine-Induced Neurotoxicity via Human Neuroblastoma Cell Line." ASM Science Journal 16 (November 5, 2021): 1–9. http://dx.doi.org/10.32802/asmscj.2021.907.
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Methamphetamine (METH) was reported to caused neurotoxicity and cell death, in vitro. Centella asiatica or ‘pegaga’ is a native tropical herb with antioxidant and neuroprotective activities. Although the effects of Centella asiatica against oxidative stress and neuronal cell death have been reported in previous studies, however, the potential effects of Centella asiatica against psychostimulant methamphetamine (METH) are limited. Therefore, this study was aimed to evaluate the effects of Centella asiatica extract (CAE) against METH on all-trans retinoic acid, RA-differentiated human neuroblastoma, SH-SY5Y cells. The RA-differentiated SH-SY5Y cells were used to resemble dopaminergic neuronal-like cells. Cell viability was quantitatively assessed by 3-(4,5-dimethylthiazol-2-yl)-2 tetrazolium bromide, MTS assay. CAE at varying concentrations from 1pg/mL to 1mg/mL significantly decreased the viability of the undifferentiated SH-SY5Y cells in a concentration-dependent manner. At 1mg/mL of CAE, significantly increased the viability of differentiated SH-SY5Y cells. Meanwhile, CAE at 100µg/mL and 1mg/mL significantly reversed the METH-induced neuronal cell death. The results revealed that promising treatment of CAE on METH-induced neurotoxicity is mediated by its high content of asiaticoside, asiatic acid, madecassoside and madecassic acid. Taken together, this study may suggest CAE as a potential therapeutic treatment for METH-induced neurotoxicity, in vitro.
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Hasbullah, N. I., Mat Zain Mazatulikhma, and N. Kamarulzaman. "Nanotoxicity of Magnesium Oxide on Human Neuroblastoma SH-SY5Y Cell Lines." Advanced Materials Research 667 (March 2013): 160–64. http://dx.doi.org/10.4028/www.scientific.net/amr.667.160.
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The use of magnesium oxide (MgO) nanoparticles in industrial applications has been raised over the last decade. However, there is limited toxicology information available regarding the effects of MgO nanoparticles. In this study, cytotoxicity and neurotoxicity of this nanoparticle on SH-SY5Y cell lines was investigated. In order to assess the cytotoxicity effect, SH-SY5Y cells were exposed to three different types of MgO nanoparticles (MgO 5, MgO 10 and MgO 24) for 24, 48 and 72 h. The concentration of nanoparticles ranges from 1nM to 1mM. Cell viability was determined by MTS assay. Neurotoxicity test was performed to determine the effects of MgO nanoparticles on human neural cells. Results indicated that MgO nanoparticles are not toxic to both undifferentiated and differentiated SH-SY5Y cells. With further exploration, the safety and health concern regarding exposure of MgO nanoparticles can be verified since the increasing of using this nanoparticle in industry over the time.
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Filiz, Ahmet Kemal, Ziad Joha, and Fatih Yulak. "Mechanism of anti-cancer effect of β-glucan on SH-SY5Y cell line." Bangladesh Journal of Pharmacology 16, no. 4 (October 1, 2021): 122–28. http://dx.doi.org/10.3329/bjp.v16i4.54872.
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Anti-cancer property of fungi derived β-glucan (Lentinula edodes) on several cancer cell lines have been reported. In this work, the SH-SY5Y cell lines were treated with various concentrations of β-glucan (62.5, 125, 250 and 500 μg/mL) and the viability of the cells was tested using the XTT assay after 24 hours. Cleaved PARP, BCL-2, 8-hydroxy-desoxyguanosine (8-oxo-dG), cleaved caspase 3, Bax, total oxidant, and total antioxidant levels in the cells were measured by commercial kits. β-Glucan significantly decreased the cell viability in SH-SY5Y cells. ELISA tests demonstrated that β-glucan therapy dramatically increased 8-oxo-dG, cleaved caspase 3, Bax, cleaved PARP, total oxidant. However, β-glucan treatment did not change the BCL-2 protein level. Altogether, β-glucan caused significant cytotoxicity in SH-SY5Y cells by inducing oxidative stress, increasing DNA damage, and ultimately increasing apoptosis.
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Xu, Lili, Jianjun Shen, Shaobing Dai, Lihong Sun, and Xinzhong Chen. "Tetramethylpyrazine Attenuated Sevoflurane-Induced Neurotoxicity by Enhancing Autophagy through GPR50/CREB Pathway in SH-SY5Y Cells." American Journal of Chinese Medicine 48, no. 04 (January 2020): 945–66. http://dx.doi.org/10.1142/s0192415x20500457.
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Tetramethylpyrazine has shown neuroprotective and axonal outgrowth-promoting effects and can improve cognitive deficit in a rat model of chronic hypoperfusion. However, the role of tetramethylpyrazine in sevoflurane-induced neurotoxicity is still vague. Therefore, this study was designed to investigate the effects and mechanisms of tetramethylpyrazine on sevoflurane-induced autophagy, apoptosis, and the expression of BACE1 and A[Formula: see text] in SH-SY5Y cells. We measured the expression levels of the apoptosis protein markers Bax and Bcl-2, autophagy protein markers Atg5 and LC3-II, BACE1, and A[Formula: see text] in SH-SY5Y cells after sevoflurane treatment and determined the effects of tetramethylpyrazine on sevoflurane-induced expression of these proteins after silencing GPR50 or Atg5 with siRNA in vitro. We found that exposure to 3.4% sevoflurane for 6 h decreased the expression of autophagy protein markers and increased the expression of the apoptosis protein markers, BACE1, and A[Formula: see text] in SH-SY5Y cells. The number of red puncta (autolysosomes) and yellow puncta (autophagosomes) in each SH-SY5Y cell decreased after transient transfection with the mRFP-GFP-LC3 expression plasmid. Silencing of GPR50 decreased the expression of pCREB, Atg5, and LC3-II, while silencing of Atg5 increased the expression of BACE1 and A[Formula: see text] in SH-SY5Y cells. Our results demonstrate that tetramethylpyrazine attenuated sevoflurane-induced neurotoxicity by enhancing autophagy through the GPR50/CREB pathway in SH-SY5Y cells.
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Acioglu, Cigdem, Mete Bora Tuzuner, Muge Serhatli, Ceyda Acilan, Betul Sahin, Emel Akgun, Zelal Adiguzel, Busra Gurel, and Ahmet Tarik Baykal. "A Proteomic Analysis of Mitochondrial Complex III Inhibition in SH-SY5Y Human Neuroblastoma Cell Line." Current Proteomics 16, no. 2 (January 4, 2019): 136–47. http://dx.doi.org/10.2174/1570164615666180713110139.
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Background and Objective: Antimycin A (AntA) is a potent Electron Transport System (ETS) inhibitor exerting its effect through inhibiting the transfer of the electrons by binding to the quinone reduction site of the cytochrome bc1 complex (Complex III), which is known to be impaired in Huntington’s Disease (HD). The current studies were undertaken to investigate the effect of complex III inhibition in the SH-SY5Y cell line to delineate the molecular and cellular processes, which may play a role in the pathogenesis of HD. Methods: We treated SH-SY5Y neuroblastoma cells with AntA in order to establish an in vitro mitochondrial dysfunction model for HD. Differential proteome analysis was performed by the nLCMS/ MS system. Protein expression was assessed by western blot analysis. Results: Thirty five differentially expressed proteins as compared to the vehicle-treated controls were detected. Functional pathway analysis indicated that proteins involved in ubiquitin-proteasomal pathway were up-regulated in AntA-treated SH-SY5Y neuroblastoma cells and the ubiquitinated protein accumulation was confirmed by immunoblotting. We found that Prothymosin α (ProT α) was downregulated. Furthermore, we demonstrated that nuclear factor erythroid 2-related factor 2 (Nrf2) protein expression was co-regulated with ProT α expression, hence knockdown of ProT α in SH-SY5Y cells decreased Nrf2 protein level. Conclusion: Our findings suggest that complex III impairment might downregulate ubiquitinproteasome function and NRF2/Keap1 antioxidant response. In addition, it is likely that downregulation of Nrf2 is due to the decreased expression of ProT α in AntA-treated SH-SY5Y cells. Our results could advance the understanding of mechanisms involved in neurodegenerative diseases.
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Liu, Lumei, Wenbin Wan, Wenjing Chen, Yuanjin Chan, Qi Shen, and Yaming Li. "Yi-Zhi-Fang-Dai Formula Protects against Aβ1–42Oligomer Induced Cell Damage via Increasing Hsp70 and Grp78 Expression in SH-SY5Y Cells." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/8591656.
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Yi-Zhi-Fang-Dai formula (YZFDF) is an experiential prescription used to cure dementia cases like Alzheimer’s disease (AD). In this study, the main effective compounds of YZFDF have been identified from this formula, and the neuroprotective effect againstAβ1–42oligomer of YZFDF has been tested in SH-SY5Y cells. Our results showed that YZFDF could increase cell viability and could attenuate endothelial reticula- (ER-) mediated apoptosis. Evidence indicated that protein folding and endothelial reticula stress (ERS) played an important role in the AD pathological mechanism. We further explored the expression of Hsp70, an important molecular chaperon facilitating the folding of other proteins, and Grp78, the marker protein of ERS in SH-SY5Y cells. Data told us that YZFDF pretreatment could influence the mRNA and protein expression of these two proteins. At last, we also found that YZFDF pretreatment could activate Akt in SH-SY5Y cells. All these above indicate that YZFDF could be a potent therapeutic candidate for AD treatment.
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Ji, Hui, Haifeng Jin, Guangwei Li, Li Jin, Xiaoxu Ren, Ying Lv, and Yuchun Wang. "Artemisinin protects against cerebral ischemia and reperfusion injury via inhibiting the NF-κB pathway." Open Medicine 17, no. 1 (January 1, 2022): 871–81. http://dx.doi.org/10.1515/med-2022-0435.
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Abstract This study investigated whether artemisinin (ART) exerts a neuroprotective effect against cerebral ischemia/reperfusion (I/R) injury. Hypoxia-glucose deprivation and reoxygenation (OGD/R) of SH-SY5Y cells were used as the I/R injury model in vitro. Cell viability was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and lactate dehydrogenase (LDH) release was measured. Cell apoptosis and apoptosis-associated protein expression were determined via flow cytometry and western blotting, respectively. The levels of glutathione peroxidase, superoxide dismutase, catalase, and malondialdehyde were determined. The secretion of tumor necrosis factor-α and interleukin-1β was measured using ELISA. The activation of the nuclear factor kappa B (NF-κB) pathway was also determined. The indicated ART concentrations (0, 25, 50, 75, and 100 μM) had no significant effect on SH-SY5Y cell viability and LDH activity. ART promoted cell viability, reduced cell apoptosis, repressed cellular inflammation, and inhibited cellular oxidative stress and NF-κB signaling pathway in OGD/R-induced SH-SY5Y cells. In addition, all the protective effects of ART on OGD/R-induced SH-SY5Y cell injury were significantly reversed by an NF-κB agonist. In conclusion, ART protects neurons from OGD/R-induced damage in vitro by inhibiting the NF-κB signaling pathway. These results suggest that ART may be a potential agent for the treatment of cerebral I/R injury.
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Coccini, Teresa, Luigi Manzo, Vittorio Bellotti, and Uliana De Simone. "Assessment of Cellular Responses after Short- and Long-Term Exposure to Silver Nanoparticles in Human Neuroblastoma (SH-SY5Y) and Astrocytoma (D384) Cells." Scientific World Journal 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/259765.
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Silver nanoparticle (AgNP, 20 nm) neurotoxicity was evaluated by an integratedin vitrotesting protocol employing human cerebral (SH-SY5Y and D384) cell lines. Cellular response after short-term (4–48 h, 1–100 μg/ml) and prolonged exposure (up to 10 days, 0.5–50 μg/ml) to AgNP was assessed by MTT, calcein-AM/PI, clonogenic tests. Pulmonary A549 cells were employed for data comparison along with silver nitrate as metal ionic form.Short-term data: (i) AgNP produced dose- and time-dependent mitochondrial metabolism changes and cell membrane damage (effects starting at 25 μg/ml after 4 h: EC50swere 40.7 ± 2.0 and 49.5 ± 2.1 μg/ml for SH-SY5Y and D384, respectively). A549 were less vulnerable; (ii) AgNP doses of ≤ 18 μg/ml were noncytotoxic; (iii) AgNO3induced more pronounced effects compared to AgNP on cerebral cells.Long-term data: (i) low AgNP doses (≤1 μg/ml) compromised proliferative capacity of all cell types (cell sensibility: SHSY5Y > A549 > D384). Colony number decrease in SH-SY5Y and D384 was 50% and 25%, respectively, at 1 μg/ml, and lower dose (0.5 μg/ml) was significantly effective towards SH-SY5Y and pulmonary cells; (ii) cell proliferation activity was more affected by AgNO3than AgNPs. In summary, AgNP-induced cytotoxic effects after short-term and prolonged exposure (even at low doses) were evidenced regardless of cell model types.