Azelnidipine inhibits H2O2-induced cell death in neonatal rat cardiomyocytes

Purpose Oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Azelnidipine is a novel dihydropyridine calcium channel blocker. Several studies have demonstrated that some dihydropyridine calcium channel blockers have antioxidant effects. We evaluated the antioxidant effects of azelnidipine compared to another dihyropyridine calcium channel blocker, nifedipine, in neonatal rat cardiomyocytes. Materials and methods We examined effects of azelnidipine and nifedipine on the H2O2-induced mitogen-activated protein kinase (MAPK) activity and cell death in neonatal rat cardiomyocytes. Results Extracellular signal-regulated protein kinases (ERK), p38 MAPK and c-Jun NH2-terminal kinases (JNK) were activated by H2O2 stimulation. Azelnidipine and nifedipine did not affect the H2O2-induced activation of ERK and p38 MAPK. In contrast, azelnidipine, but not nifedipine, inhibited the H2O2-induced JNK activation. The numbers of viable cell were significantly decreased by H2O2 treatments (65.8 +/- 4.11% of control, P < 0.0001). Azelnidipine, but not nifedipine, inhibited the H2O2-induced cell death (azelnidipine: 76.0 +/- 4.66% of control, P < 0.05; nifedipine: 70.7 +/- 4.01% of control, P=0.32). Conclusion Azelnidipine inhibited the H2O2-induced JNK activation and cardiac cell death. Azelnidipine may have cardioprotective effects against oxidative stress.