ArticleEndocrine2012
Mitochondrial reactive oxygen species (ROS) inhibition ameliorates palmitate-induced INS-1 beta cell death.
Article in Endocrine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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50 citing papers in PubMed, 80 citations in OpenAlex.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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