Nifedipine Protects INS-1 β-Cell from High Glucose-Induced ER Stress and Apoptosis
AbstractSustained 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.
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Wang, Y.; Gao, L.; Li, Y.; Chen, H.; Sun, Z. Nifedipine Protects INS-1 β-Cell from High Glucose-Induced ER Stress and Apoptosis. Int. J. Mol. Sci. 2011, 12, 7569-7580.
Wang Y, Gao L, Li Y, Chen H, Sun Z. Nifedipine Protects INS-1 β-Cell from High Glucose-Induced ER Stress and Apoptosis. International Journal of Molecular Sciences. 2011; 12(11):7569-7580.Chicago/Turabian Style
Wang, Yao; Gao, Lu; Li, Yuan; Chen, Hong; Sun, Zilin. 2011. "Nifedipine Protects INS-1 β-Cell from High Glucose-Induced ER Stress and Apoptosis." Int. J. Mol. Sci. 12, no. 11: 7569-7580.