L-精氨酸-一氧化氮通路对异丙肾上腺素诱导的大鼠心肌肥大的影响  

Inhibitory effects of L-arginine-nitric oxide pathway on cardiac hypertrophy induced by isoproterenol

作　　者：林岩[1] 肖锋刚[1] 李振涛[1] 潘程捷[1] 黄旭[1] 刘博婵[1] 喻庆安[1] 刘博[1] 

机构地区：[1]齐齐哈尔医学院病理生理教研室,黑龙江齐齐哈尔161006

出　　处：《中国现代医学杂志》2009年第24期3692-3696,共5页China Journal of Modern Medicine

基　　金：黑龙江省普通高等学校青年学术骨干支持计划项目(No:1153G055);黑龙江省青年科学技术专项基金(No:QC07C109);齐齐哈尔市科技计划项目

摘　　要：目的探讨L-精氨酸对心肌肥厚的影响及相关机制。方法皮下注射异丙肾上腺素(ISO)复制大鼠心肌肥厚模型,L-精氨酸作为干预因素,检测心脏重量参数,心肌组织胶原染色,心房利钠肽(ANP)的转录水平,观察L-精氨酸对心肌肥大的影响;不同时间段,应用Western blot结合图像分析系统,检测各组大鼠心肌组织内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)的蛋白表达水平;检测血清NO含量和NOS活性。结果皮下注射ISO7d后,心脏重量参数增加,ANP mRNA表达增加;L-精氨酸抑制心肌肥大,随着L-精氨酸作用时间延长,血清NOS活性增强,NO含量增加。同时,iNOS蛋白表达下调,eNOS蛋白表达上调。结论L-精氨酸可以抑制病理性心肌肥大,这与其调节iNOS和eNOS表达,增加NO含量有关。【Objective】To explore the role and possible mechanism of L-arginine on pathological cardiac hypertrophy induced by isoproterenol （ISO）.【Methods】Hypertrophic model of rats was established using ISO.Pretreated with L-arginine,hypertrophy status of rats were determined by hypertrophy coefficient,collagen content and the expression of ANP mRNA.Western blot was performed to detect the expressions of inducible nitric oxide synthase （iNOS） and endothelial nitric oxide synthase （eNOS）,the activity and level of NOS and NO in serum were observed.【Results】Hypertrophy coefficient and expression of ANP mRNA increased significantly after injection of ISO for 7 days,moreover cardiac muscle fibres become thick and disorganized.Pretreated with L-arginine,above index were decreased.Meanwhile,the concentration of plasm NO content and NOS activity were increased,the expression of iNOS was downregulated and the expression of eNOS was upregulated.【Conclusion】Exogenous L-arginine can inhibit cardiac hypertrophy through regulating the expressions of iNOS and eNOS to increasing NO content.

关 键 词：心肌肥厚 L-精氨酸 一氧化氮 

分 类 号：R363[医药卫生—病理学]