• Yuting Jiang, Benson O A Botchway, Zhiying Hu, and Marong Fang.
• Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou, China.
• Neuroscience. 2019 Jul 15; 411: 11-22.

AbstractIndividuals continuously confronted with various stresses in modern life generate high levels of cortisol (corticosterone in rodents), the major glucocorticoid secreted by adrenal gland when hypothalamic-pituitary-adrenal axis is activated. Chronic stress can induce constant release of glucocorticoid and cause many serious health problems, such as mental disorders, cardiovascular diseases and autoimmune diseases. Many studies have suggested the neurotoxic effect of corticosterone is mediated through increased oxidative stress and apoptosis. Although SIRT1 has been shown to be protective against conditions such as DNA damage and oxidative stress through autophagy regulation, the exact role of SIRT1 and autophagy in corticosterone-induced stress is still unclear. By utilizing a cellular stress model of exposing cells to corticosterone, our study found that there were a dose-dependent decrease in SIRT1 and an increase in LC3B II/I expressions with increasing concentrations of corticosterone. In combination with SIRT1 overexpression and knockdown plasmids, the regulation of SIRT1 expression in vitro demonstrated that SIRT can inhibit corticosterone-induced autophagy and enhance cell apoptosis. These findings might help us better understand the role of SIRT1 and autophagy activation in chronic stress.Copyright © 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

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