蛋白激酶C在精氨酸加压素诱导的心肌成纤维细胞诱导型一氧化氮合酶-一氧化氮系统活性增高中的作用

Roles of protein kinase C in inducible nitric oxide synthase -nitric oxide system activity increase in arginine vasopressin-induced cardiac fibroblasts

目的:观察蛋白激酶C(PKC)在精氨酸加压素(AVP)诱导下仔鼠心肌成纤维细胞(CFs)诱导型一氧化氮合酶(i NOS)-一氧化氮(NO)系统活性增高中的作用。方法:胰酶消化法分离培养Sprague-Dawley仔鼠CFs,硝酸还原酶法、分光光度法和逆转录-聚合酶链式反应(RT-PCR)检测CFs NO含量、一氧化氮合酶(NOS)活性和i NOS mRNA表达。结果:AVP显著提高CFs i NOS-NO系统活性;PKC抑制剂chelerythrine剂量依赖性地抑制AVP对CFs i NOS-NO系统活性的提高作用,其中10-6mol/L chelerythrine可将AVP诱导下CFs i NOS-NO系统活性抑制到与基础状态近似水平。结论:PKC参与了AVP诱导下CFs i NOS-NO系统活性的提高,PKC有可能成为阻断或逆转心肌纤维化新的干预靶点。

Objective：To explore the role of protein kinase C （PKC） in inducible nitric oxide synthase （iNOS）nitric oxide （NO） system activity increase in arginine vasopressin（AVP）-induced rat cardiac fibroblasts（CFs）. Method：CFs were isolated by trypsin digestion method. Nitric acid reductase method, spectrophotometry and reverse transcription-polymerase chain reaction（RT-PCR） were used to detect NO contents, NOS activity and iNOS mRNA expression. Result： AVP significantly increased iNOS-NO system activity in CFs. PKC inhibitor chelerythrine inhibited iNOS-NO system activity increase induced by AVP in a concentration-dependent manner and 10-~ mol/L chelerythrine could decreased iNOS-NO system activity to control level. Conclusion： PKC is involved iNOS- NO system activity increase in AVP-induced CFs, and PKC may be a new target in prevention and reversion of myocardial fibrosis.