Nifedipine protects INS-1 β-cell from high glucose-induced ER stress and apoptosis

Abstract

Sustained high concentration of glucose has been verified toxic to β-cells. Glucose augments Ca 2+-stimulated insulin release in pancreatic β-cells, but chronic high concentration of glucose could induce a sustained level of Ca 2+ 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 Ca 2+ 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 μnifedipine inhibited Ca 2+ release to protect β-cells from high glucose-induced endoplasmic reticulum stress and apoptosis. These results indicated that inhibition of Ca 2+ over-accumulation might provide benefit to attenuate islet β-cell decompensation in a high glucose environment. © 2011 by the authors; licensee MDPI, Basel, Switzerland.