Sulfaphenazole Attenuates Myocardial Cell Apoptosis Accompanied With Cardiac Ischemia–Reperfusion by Suppressing the Expression of BimEL and Noxa

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  • Ishihara Yasuhiro
    Graduate School of Integrated Arts and Sciences, Hiroshima University, Japan Laboratory of Pharmacology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Japan Graduate School of Integrated Arts and Sciences, Hiroshima University, Japan Laboratory of Pharmacology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Japan
  • Shimamoto Norio
    Laboratory of Pharmacology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Japan Laboratory of Pharmacology, Kagawa School of Pharmaceutical Sciences, Tokushima Bunri University, Japan

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  • Sulfaphenazole Attenuates Myocardial Cell Apoptosis Accompanied With Cardiac Ischemia^|^ndash;Reperfusion by Suppressing the Expression of BimEL and Noxa

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Abstract

We previously reported the administration of a potent cytochrome P450 inhibitor, sulfaphenazole (SPZ), to suppress oxidative stress and the extension of myocardial infarct size in a rat model of cardiac ischemia–reperfusion (I/R). The aim of this study was to investigate the effects of SPZ on the myocardial cell apoptosis induced by I/R in rats. I/R injury was evoked by ligation of the left anterior descending coronary artery for 1 h, followed by reperfusion for 3 h. TUNEL-positive nuclei were detected and nucleosomal DNA fragmentation was observed 3 h after reperfusion. The administration of SPZ largely suppressed the cardiac DNA fragmentation induced by I/R. A pan-caspase inhibitor, z-VAD-fmk, had no effect on DNA fragmentation. Caspase-3/7 was not activated 3 h after reperfusion. Decreases in the mitochondrial membrane potential and cytochrome c release from the mitochondria to cytosol were detected 3 h after reperfusion. The expression levels of BimEL and Noxa were elevated 3 h after reperfusion. These phenomena were suppressed by the administration of SPZ. Taken together, treatment with SPZ could attenuate the myocardial cell apoptosis accompanied with I/R by inhibiting the mitochondrial dysfunction due to decreases in the expression of BimEL and Noxa.

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