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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 observe the activity of protein kinase C (PKC) induced by arginine vasopressin (AVP) on the inducible nitric oxide synthase (iNOS) - nitric oxide (NO) activity in cultured rat cardiac fibroblasts Increase in the role. Methods: CFs, nitrate reductase, spectrophotometry and reverse transcription polymerase chain reaction (RT-PCR) were used to detect the contents of NO and the content of nitric oxide synthase (NOS) in CFs of Sprague-Dawley pups isolated and cultured by trypsin digestion. Activity and i NOS mRNA expression. Results: AVP significantly increased the activity of CFs i NOS-NO system. PKC inhibitor chelerythrine inhibited AVP-induced CFs i NOS-NO system activity in a dose-dependent manner. Among them, 10-6 mol / L chelerythrine could induce CFs i NOS The activity of -NO system is inhibited to approximately the same level as the basal state. CONCLUSION: PKC is involved in the increase of activity of CFs in NOS-NO system induced by AVP. PKC may be a new target for blocking or reversing myocardial fibrosis.