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Mitochondrial reactive oxygen species (ROS) inhibition ameliorates palmitate-induced INS-1 beta cell death

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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.

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Acknowledgment

This study was supported by the National Natural Science Foundation of China (No. 30872727 and No. 81170757).

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Correspondence to Qing Su.

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Lin, N., Chen, H., Zhang, H. et al. Mitochondrial reactive oxygen species (ROS) inhibition ameliorates palmitate-induced INS-1 beta cell death. Endocrine 42, 107–117 (2012). https://doi.org/10.1007/s12020-012-9633-z

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