title: Mitochondrial reactive oxygen species (ROS) inhibition ameliorates palmitate-induced INS-1 beta cell death.
abstract: The purpose of this study is to explore the possible link between oxidative stress and endoplasmic reticulum (ER) stress in palmitate (PA) induced apoptosis of INS-1 cells, and to figure out the main source of reactive oxygen species (ROS) and the effect of ROS inhibition on the level of ER stress. In this study, INS-1 cells were exposed to PA and oleate for the indicated times. Cell viability and apoptosis were measured by MTT and ELISA; ROS was detected by the probe DCFH-DA and MitoSOX Red using flow cytometer; and the ER stress-related chaperones were measured by western blotting and real time PCR. The level of JNK phosphorylation was also measured by western blotting. The results showed that, in PA-treated cells, apoptosis increased in a dose-dependent way. ROS generation was mainly increased through mitochondrion, and ROS inhibition reduced the expression of some ER chaperones and transcription factors levels. Also, inhibition of JNK phosphorylation ameliorated PA-induced apoptosis. It is concluded that, ROS inhibition, especially inhibiting the ROS from mitochondria, may reduce the expression of some ER stress-related effectors and show a protective role in PA-induced pancreatic beta-cell apoptosis.
authors.affiliation: Department of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, 1665, KongJiang Road, Shanghai, 200092, China.
authors.forename: Ning
authors.initials: N
authors.lastname: Lin
authors.forename: Hanbei
authors.initials: H
authors.lastname: Chen
authors.forename: Hongmei
authors.initials: H
authors.lastname: Zhang
authors.forename: Xiaoyu
authors.initials: X
authors.lastname: Wan
authors.forename: Qing
authors.initials: Q
authors.lastname: Su
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000378:metabolism; D016923:Cell Death / Q000187:drug effects; D002478:Cells, Cultured; D004353:Drug Evaluation, Preclinical; D004357:Drug Synergism; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D005230:Fatty Acids, Nonesterified / Q000494:pharmacology; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D008928:Mitochondria / Q000378:metabolism; D019308:Palmitic Acid / Q000494:pharmacology*; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D005230:Fatty Acids, Nonesterified; D017382:Reactive Oxygen Species; D019308:Palmitic Acid; C505410:Casp3 protein, rat; D053148:Caspase 3