NO对新生大鼠心肌细胞PKC活性的影响

利用培养新生大鼠心肌细胞，检测NO前体L-精氨酸(L-arginine,L-Arg)和NO供体硝普钠(sodium nitroprusside,SNP)对PKC活性的影响，并探讨内、外源性NO在PKC激动剂佛波指(phorbol 12-myristate 13-acetate,PMA)激活PKC中的作用.实验结果表明：培养基中加入L-Arg，PKC活性呈剂量依赖性降低；用L-Arg进行预处理，30 min后加入PMA，PKC活性明显降低，与单纯PMA组相比有显著差异；NOS抑制剂L-NAME本身对基础状态PKC活性无明显影响，但可阻断L-Arg对上述2个效应的影响；培养液中加入NO供体SNP，PKC活性呈剂量依赖性降低；用SNP预处理心肌细胞，5 min后加入PMA，PKC活性与单纯PMA组相比有显著性差异.以上结果表明，内、外源性NO均具有剂量依赖性抑制PKC活性的作用，PKC可能是NO对心肌细胞作用的胞内信号传导通路的关键部位或重要信号分子之一；L-Arg通过NOS先生成NO，NO再对PKC起抑制作用.

The Role of Nitric Oxide on Protein Kinase C Activity in Neonatal Rat Cardiomyocytes

The effect of endogenous and exogenous nitric oxide(NO) on protein kinase(PKC) activity in cultured neonatal rat cardiomyocytes was examined.The results were as following:Activity of PKC was decreased by NO precursor L-arginine(L-Arg) (10^-5～10^-2 mol/L,30 min) and NO donor sodium nitroprusside (SNP)(10^-6～10^-3 mol/L,5 min)in a dose-dependent manner in cultured neonatal rat cardiomyocytes.Activity of PKC increased by a PKC activator phorbol 12-myristate 13-acetate(PMA)(10-5mol/L,15 min) was impaired by a NO precursor L-Arg and a exogenous NO donor SNP.NG-nitro-L-argingie methyl ester(L-NAME),a nitric oxide synthase (NOS) blocker,itself had no effect on the PKC activity of cultured neonatal rat cardiomyocytes,but may inhibite the role of PKC activity induced PMA.These results indicate that PKC was decreased by endogenous and exogenous NO in a dose-dependent manner.The role of NO on rat cardiomyocytes intracellular signaling transduction pathway may be controlled through PKC.PKC may turn into key site or important signaling element of this effect.