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자료유형
학술저널
저자정보
Lingappa Sivakumar (Centre of Advanced Study in Marine Biology Faculty of Marine Sciences Annamalai University Parangip) Shivakumar Muthugounder Subramanian (Molecular Entomology Lab Department of Biotechnology Periyar University Salem 636011 Tamilnadu Indi) Manivasagam Thamilarasan (Department of Biochemistry & Biotechnology Faculty of Science Annamalai University) Somasundaram Somasundaram Thirugnanasambandan (Centre of Advanced Study in Marine Biology Faculty of Marine Sciences Annamalai University Parangip) Seedevi Palaniappan (Department of Environmental Science Periyar University Salem 636011 Tamilnadu India)
저널정보
한국미생물생명공학회 Journal of Microbiology and Biotechnology Journal of Microbiology and Biotechnology 제31권 제6호
발행연도
2021.1
수록면
867 - 874 (8page)

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Epalrestat (EPS) is a brain penetrant aldose reductase inhibitor, an approved drug currently used for the treatment of diabetic neuropathy. At near-plasma concentration, EPS induces glutathione biosynthesis, which in turn reduces oxidative stress in the neuronal cells. In this study, we found that EPS reduces neurodegeneration by inhibiting reactive oxygen species (ROS)-induced oxidative injury, mitochondrial membrane damage, apoptosis and tauopathy. EPS treatment up to 50 μM did not show any toxic effect on SH-SY5Y cell line (neuroblastoma cells). However, we observed toxic effect at a concentration of 100 μM and above. At 50 μM concentration, EPS showed better antioxidant activity against H2O2 (100 μM)-induced cytotoxicity, ROS formation and mitochondrial membrane damage in retinoic acid-differentiated SH-SY5Y cell line. Furthermore, our study revealed that 50 μM of EPS concentration reduced the glycogen synthase kinase-3 β (GSK3-β) expression and total tau protein level in H2O2 (100 μM)-treated cells. Findings from this study confirms the therapeutic efficacy of EPS on regulating Alzheimer's disease (AD) by regulating GSK3- β and total tau proteins phosphorylation, which helped to restore the cellular viability. This process could also reduce toxic fibrillary tangle formation and disease progression of AD. Therefore, it is our view that an optimal concentration of EPS therapy could decrease AD pathology by reducing tau phosphorylation through regulating the expression level of GSK3-β.

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