Glycitin Induced Autophagy to Clear Amyloid Beta and Protects Neuronal Cell in Alzheimer?s Disease
Department of Neurology, Nankai University Affiliated Nankai Hospital, Nankai, Tianjin 300100, China
H. Wang, Department of Neurology, Nankai University Affiliated Nankai Hospital, Nankai, Tianjin 300100, China, E-mail: email@example.com
Accumulation of amyloid beta and its toxicity are the common features in Alzheimer’s disease. Autophagy plays an important role in development and progression of Alzheimer’s disease by causing selfdegradation of accumulated amyloid beta from neurons. Glycitin has been found as major phytochemical constituent of soybean, which shows neuroprotective function in Alzheimer’s disease. The present study aims to explore the role of glycitin in clearance of amyloid beta and reducing amyloid beta toxicity in neuronal cells. The human microglial cells 3 and neuroblastoma cell SHSY-5Y were used in the current study. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay was used to access cell viability and neuroprotection. Western blotting was used to determine expression levels of different proteins. Autophagosome marker (light chain 3) was studied using confocal microscopy. Clearance of amyloid beta was studied using confocal microscopy and enzyme-linked immunosorbent assay. We reported that glycitin induces autophagy in human microglial cells 3 cells through phosphatidylinositol 3-kinase/protein kinase B pathway. Glycitin clears amyloid beta and its associated toxicity in neuroblastoma SHSY-5 cells. Furthermore, light chain 3 knockdown inhibits glycitin associated neuroprotective effects in neuroblastoma SHSY-5 cells. We conclude that glycitin can be used as an alternate strategy for curing Alzheimer’s disease.