International Journal of Molecular Sciences | |
Nifedipine Protects INS-1 β-Cell from High Glucose-Induced ER Stress and Apoptosis | |
Yao Wang2  Lu Gao1  Yuan Li2  Hong Chen2  | |
[1] Key Laboratory of Human Functional Genomics of Jiangsu Province, Clinical Diabetes Centre of Jiangsu Province, Nanjing Medical University, Nanjing 210029, China; E-Mail:;Department of Endocrinology, Zhongda Hospital, Institute of Diabetes, Southeast University, No.87 Dingjiaqiao Road, Nanjing, Jiangsu 210009, China; E-Mails: | |
关键词: nifedipine; Ca2+ homeostasis; β-cell; endoplasmic reticulum stress; apoptosis; high glucose; | |
DOI : 10.3390/ijms12117569 | |
来源: mdpi | |
【 摘 要 】
Sustained high concentration of glucose has been verified toxic to β-cells. Glucose augments Ca2+-stimulated insulin release in pancreatic β-cells, but chronic high concentration of glucose could induce a sustained level of Ca2+ in β-cells, which leads to cell apoptosis. However, the mechanism of high glucose-induced β-cell apoptosis remains unclear. In this study, we use a calcium channel blocker, nifedipine, to investigate whether the inhibition of intracellular Ca2+ concentration could protect β-cells from chronic high glucose-induced apoptosis. It was found that in a concentration of 33.3 mM, chronic stimulation of glucose could induce INS-1 β-cells apoptosis at least through the endoplasmic reticulum stress pathway and 10 μM nifedipine inhibited Ca2+ release to protect β-cells from high glucose-induced endoplasmic reticulum stress and apoptosis. These results indicated that inhibition of Ca2+ over-accumulation might provide benefit to attenuate islet β-cell decompensation in a high glucose environment.
【 授权许可】
CC BY
© 2011 by the authors; licensee MDPI, Basel, Switzerland.
【 预 览 】
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