20-HETE Induce Apoptosis Via Protein Kinase C And NADPH Oxidase In Neonatal Rat Cardiomyocytes

20-hydroxyeicosatetraenoic acid (20-HETE) is a primary product ofcytochrome P-4504A (CYP4A) metabolism of arachidonic acid, and it may play arole in the cardiovascular system. It is reported that20-HETE is increasing duringischemia-reperfusion, whereas the inhibitor of20-HETE can decrease the apoptosisof cardiac myocytes cells during ischemia.This study aims to discover themechanism of20-HETE-induced apoptosis in cardiac myocytes, and the effect of20-HETE on apoptosis in cardiac myocytes cells was examined by FACScan flowcytometer. In this study, we found that20-HETE will induce cardiomyocytes cellsapoptosis in a concentration-dependent manner. Furthermore, the apoptosis processwill be attenuated by chelerythrine, a specific PKC inhibitor, and increased byPMA, a PKC activator. These results suggested that PKC may be involved in20-HETE-induced apoptosis in cardiomyocytes cells. To study the mechanism of20-HETE-induced apoptosis mediated by PKC, the inhibitors of NADPH oxidasewas treated to cardiomyocytes, which could significantly the20-HETE-inducedapoptosis. Thus, these results indicated that NADPH oxidizes maybe also involvedin cell apoptosis induced by20-HETE. In summary, we found that20-HETE couldinduced cardiomyocytes apoptosis via PKC， NADPH oxidase. The20-HETE-induced apoptosis could contribute to the cytochrome P450v-hydroxylase-dependent cardiac injure during cardiac ischemia–reperfusion.