文献类型：期刊文献

英文题名：Inhibitory effects of curcumin on H2O2-induced cell damage and APP expression and processing in SH-SY5Y cells transfected with APP gene with Swedish mutation

作者：Song, Xi-Jun[1];Zhou, He-Yan[1];Sun, Ya-Xuan[1];Huang, Han-Chang[1]

第一作者：Song, Xi-Jun

通讯作者：Huang, HC[1]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, 197 Beitucheng West Rd, 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：2020

卷号：47

期号：3

起止页码：2047-2059

外文期刊名：MOLECULAR BIOLOGY REPORTS

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000516229500003)】；

基金：This study was supported by the National Natural Science Foundation of China (31471587), the Premium Funding Project for Academic Human Resources Development in Beijing Union University (BPHR2018CZ02), and Opening Project of Beijing Key Laboratory of Bioactive Substances and Functional Foods Beijing Key Laboratory (2019SPKF01).

语种：英文

外文关键词：Alzheimer's disease; Amyloid-beta protein precursor (APP); Amyloid-beta peptide; Cell damage; Hydrogen peroxide (H2O2); Curcumin; Mitochondrial stress

摘要：Alzheimer's disease (AD) is a neurodegenerative disorder, and the pathological mechanism of the disease is still far to understand. According to the amyloid cascade hypothesis in AD, Amyloid-beta (A beta) is considered as a key substance that contributes AD development. A beta is a beta-cleaving product from Amyloid-beta protein precursor (APP). Mutations of APP including APP(KM670/671670NL) (Swedish mutation) result in A beta overproduction and the development of early-onset familial AD. Increase of oxidative stress and damage also occurs in early stage of AD. In this study, we used a SH-SY5Y cell line that stably expresses APP gene with Swedish mutation (SH-SY5Y-APPswe), and the inhibitory effects of curcumin on H2O2-induced cell damage and APP processing were investigated. Cells were treated with curcumin (0 similar to 5 mu M) for 4 h before hydrogen peroxide (H2O2). Cell growth was detected with CCK-8 assay, and cell damage was determined through the evaluation of release of lactate dehydrogenase (LDH) from the cytosol to the culture medium and the morphological change of nucleus. The ability of mitochondrial stress and the depolarization of mitochondrial membrane potential were assayed through the measuring the oxygen consumption rate (OCR) and the green/red fluorescence ratio of JC-1 dye respectively. The protein levels of APP, sAPP alpha, sAPP beta, and BACE1 were analyzed with Western blot assay. A beta production was measured with enzyme-linked immunosorbent assay (ELISA). The results indicated that curcumin inhibits H2O2-induced decrease of cell growth and cell damage. Curcumin attenuates H2O2-induced damage on the ability to mitochondrial oxidative phosphorylation and membrane potential. Curcumin inhibits H2O2-induced increase of APP cleavage through beta-cleavage pathway and of intracellular A beta production. These results imply that curcumin can be used to treat AD through inhibiting oxidative damage-induced APP beta-cleavage and intracellular A beta generation.