文献类型：期刊文献

英文题名：Chitooligosaccharides Attenuate Cu2+-Induced Cellular Oxidative Damage and Cell Apoptosis Involving Nrf2 Activation

作者：Huang, Han-Chang[1,2];Hong, Liang[1];Chang, Ping[1,2];Zhang, Jiao[1];Lu, Shu-Yan[1,2];Zheng, Bo-Wen[1,2];Jiang, Zhao-Feng[1,2]

第一作者：黄汉昌

通讯作者：Huang, HC[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Beijing Union Univ, Coll Arts & Sci, Beijing 100191, Peoples R China

第一机构：北京联合大学应用文理学院|北京联合大学生物化学工程学院

通讯机构：[1]corresponding author), Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, 197 Beitucheng West Rd, 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：2015

卷号：27

期号：4

起止页码：411-420

外文期刊名：NEUROTOXICITY RESEARCH

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000352298900005)】；

基金：This study was supported by the National Natural Science Foundation of China (31471587) and the Scientific Research Common Program of Beijing Municipal Commission of Education (SQKM201411417003).

语种：英文

外文关键词：Alzheimer's disease; Chitooligosaccharides; Cu2+; Nrf2; Oxidative damage

摘要：Alzheimer's disease (AD) is one of the common neurodegenerative diseases. Increase of labile copper pool plays an important role in the pathogenesis of AD. Nrf2(NF-E2-related factor-2)-ARE (antioxidant response element) signaling is an important intracellular manner to defend against oxidative stress. In this study, we used SH-SY5Y cells as a model of neuron to test the effect of chitooligosaccharides (COSs) on Cu2+-induced oxidative damage. SH-SY5Y cells were treated with different concentrations of COSs (100-800 mg/L) before incubated with Cu2+. Cell viability and cell damage and apoptosis were assessed. Both extracellular H2O2 and intracellular ROS were measured and the relative levels of Nrf2, phosphorylated Nrf2, and HO-1 were analyzed by Western blotting, and further HO-1 mRNA was relatively quantified by real-time quantitative PCR. The results indicated that Cu2+-induced decrease of cell viability and increase of LDH release. In cell-free solution, COSs alone or with Cu2+ cannot scavenge O-2 (-); however, COSs downregulate the levels of cellular oxidative stress and activated Caspase-3 induced by Cu2+. Further, the levels of pSer40-Nrf2 protein and both the transcription and the translation of HO-1 gene are dramatically increased in COSs-protective group compared with Cu2+ damage group. Therefore, these results indicate that Nrf2 activation might be involved in the protection of COSs against Cu2+-induced cellular oxidative damage. COSs contribute to the attenuation of oxidative damage and could be used as a nutritional agent for AD treatment.