Azelnidipine inhibits H2O2-induced cell death in neonatal rat cardiomyocytes.

Abstract:

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.

journal_name

Cardiovasc Drugs Ther

authors

Koyama Y,Takeishi Y,Takahashi H,Shishido T,Arimoto T,Niizeki T,Harada M,Suzuki S,Kitahara T,Sasaki T,Kubota I

doi

10.1007/s10557-007-6008-4

subject

Has Abstract

pub_date

2007-02-01 00:00:00

pages

69-72

issue

1

eissn

0920-3206

issn

1573-7241

journal_volume

21

pub_type

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