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Updated: Jul 16, 2026
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Published on: October 19, 2013
Azelnidipine inhibits H2O2-induced cell death in neonatal rat cardiomyocytes
Yo Koyama1, Yasuchika Takeishi, Hiroki Takahashi
1Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, 2-2-2 Iida-Nishi, Yamagata, 990-9585, Japan. takeishi@med.id.yamagata-u.ac.jp
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 H(2)O(2)-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 NH(2)-terminal kinases (JNK) were activated by H(2)O(2) stimulation. Azelnidipine and nifedipine did not affect the H(2)O(2)-induced activation of ERK and p38 MAPK. In contrast, azelnidipine, but not nifedipine, inhibited the H(2)O(2)-induced JNK activation. The numbers of viable cell were significantly decreased by H(2)O(2) treatments (65.8 +/- 4.11% of control, P < 0.0001). Azelnidipine, but not nifedipine, inhibited the H(2)O(2)-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 H(2)O(2)-induced JNK activation and cardiac cell death. Azelnidipine may have cardioprotective effects against oxidative stress.
