Nifedipine Protects INS-1 β-Cell from High Glucose-Induced ER Stress and Apoptosis

International Journal of Molecular Sciences

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.