文献类型：期刊文献

英文题名：Curcumin Inhibits Cell Damage and Apoptosis Caused by Thapsigargin-Induced Endoplasmic Reticulum Stress Involving the Recovery of Mitochondrial Function Mediated by Mitofusin-2

作者：Zhou, He-Yan[1,2];Sun, Yu-Ying[1,2];Chang, Ping[1,2];Huang, Han-Chang[1,2]

通讯作者：Huang, HC[1];Huang, HC[2]

机构：[1]Beijing Union Univ, Beijing Key Lab Bioact Subst & Funct Foods, Beijing 100191, Peoples R China;[2]Beijing Union Univ, Inst Funct Factors & Brain Sci, Beijing 100023, 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, Beijing 100191, Peoples R China;[2]corresponding author), Beijing Union Univ, Inst Funct Factors & Brain Sci, Beijing 100023, Peoples R China.|[11417]北京联合大学;[114172]北京联合大学应用文理学院;[1141726]北京联合大学生物化学工程学院;

年份：2022

卷号：40

期号：2

起止页码：449-460

外文期刊名：NEUROTOXICITY RESEARCH

收录：;Scopus(收录号：2-s2.0-85125047943);WOS:【SCI-EXPANDED(收录号:WOS:000759373200002)】；

基金：This study was supported by the Academic Research Projects of Beijing Union University (JZ10202001, XP202008, and ZK70202101).

语种：英文

外文关键词：Curcumin; Endoplasmic reticulum stress (ERS); Mitofusin-2 (Mfn2); Mitochondrial dysfunction; SH-SY5Y cells; Thapsigargin

摘要：Endoplasmic reticulum stress (ERS) and mitochondrial dysfunction have been suggested to relate with the pathology of Alzheimer's disease (AD). However, their cross-talk is needed to investigate further. Mitofusin-2 (Mfn2) is a member of mitochondria-associated membrane (MAM), which connects endoplasmic reticulum (ER) and mitochondria. This study investigated the protective effect of curcumin on thapsigargin (TG)-induced ERS and cell apoptosis and the role of Mfn2 on mitochondrial dysfunction. The cell viability of SH-SY5Y cells was decreased and cell damage and apoptosis were increased in a concentration-dependent manner when cells were treated with TG. TG upregulated the protein levels of GRP78, pSer981-PERK, and pSer51-eIF2 alpha. Curcumin attenuated TG-induced damage on cell viability and apoptosis and downregulated the protein levels of GRP78, pSer981-PERK, and pSer51-eIF2 alpha. TG caused the increases in intracellular reactive oxygen species (ROS) and in the protein levels of pSer40-Nrf2 and hemoglobin oxygenase 1 (HO-1). Curcumin decreased the TG-induced intracellular ROS but did not alter the protein levels of pSer40-Nrf2 and HO-1. TG resulted in the upregulation on Mfn2 expression and mitochondrial spare respiratory capacity but the downregulation on mitochondrial basal respiration and ATP production. Curcumin attenuated the TG-induced Mfn2 expression and mitochondrial stress. When Mfn2 was silenced by shRNA interference, curcumin failed to recovery the TG-damaged mitochondrial function. In general, the TG-induced ERS trigged mitochondrial dysfunction and cell apoptosis. Curcumin attenuates TG-induced ERS and the cell damage and apoptosis. Mfn2 is required for curcumin's protection against the TG-induced damage on mitochondrial functions.