文献类型：期刊文献

英文题名：Protective Effect of Chitosan Oligosaccharide against Hydrogen Peroxide-Mediated Oxidative Damage and Cell Apoptosis via Activating Nrf2/ARE Signaling Pathway

作者：Zhang, Xiaoxia[1];Liang, Shuang[1];Gao, Xiaohan[1];Huang, Hanchang[1];Lao, Fengxue[1];Dai, Xueling[1]

第一作者：Zhang, Xiaoxia

通讯作者：Dai, XL[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Food, Beijing 100191, Peoples R China

第一机构：北京联合大学生物化学工程学院|北京联合大学应用文理学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Food, Beijing 100191, Peoples R China.|[1141726]北京联合大学生物化学工程学院;[11417]北京联合大学;[114172]北京联合大学应用文理学院;

年份：2021

卷号：39

期号：6

起止页码：1708-1720

外文期刊名：NEUROTOXICITY RESEARCH

收录：;Scopus(收录号：2-s2.0-85116433119);WOS:【SCI-EXPANDED(收录号:WOS:000704937200001)】；

基金：This research was supported by grants from the Beijing Natural Science Foundation (6164030), 2019 Basic Research Projects of Beijing Union University, Beijing Key Laboratory of Bioactive Substances and Functional Foods Research Project, the Academic Research Projects of Beijing Union University (ZK80202102, XP202008, ZK40201902), and Graduate Funding Project of Beijing Union University.

语种：英文

外文关键词：Chitosan oligosaccharide; Oxidative stress; Cell apoptosis; Nrf2; MAPKs

摘要：Chitosan oligosaccharide (COS), hydrolyzed and deacetylated from chitosan, has been reported to possess varieties of biological activities. Alzheimer's disease (AD) is a multifactorial progressive neurodegenerative disorder characterized by cognitive decline and memory loss, where oxidative stress was reported to be an overwhelming cause of the occurrence of AD. We have previously reported that COS could significantly decrease cell death, ROS generation, and lipid peroxidation, though the potential mechanism was yet to be determined. This study was designed to investigate the neuroprotective effect of COS against hydrogen peroxide (H2O2)-induced oxidative stress and apoptosis in neuronal SH-SY5Y cells. Our results indicated that COS could dose-dependently scavenge H2O2 in the cell-free systems. Accordingly, COS markedly decreased H2O2-induced cell apoptosis and intracellular ROS generation, while increased antioxidant capacity in SH-SY5Y cells. Further, COS significantly reduced the expression of Bax and upregulated Bcl-2. The mRNA and protein expression levels of nuclear Nrf2, heme oxygenase 1 (HO-1), and NAD(P)H: quinone oxidoreductase 1 (NQO1) were significantly increased upon COS treatment. Moreover, Nrf2-siRNA evidently reversed the promotive effect of COS on expression levels of HO-1 and NQO1, and ARE-driven transcriptional activity as determined by double-luciferase reporter gene assay. Besides, COS reversed H2O2-mediated increased phosphorylation of ERK1/2 and p38 MAPK. In conclusion, our findings indicate that COS could protect SH-SY5Y cells from oxidative damage and apoptosis via regulating Nrf2/ARE signaling pathway, which may provide new applications for the prevention and treatment of AD.