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Atorvastatin Attenuates Myocardial Hypertrophy Induced by chronic Intermittent Hypoxia In Vitro Partly through miR-31/PKcε Pathway

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current Medical Science 2018年第3期38卷 405-412页

作者： Jie REN Wei LIU Guang-cai LI Meng JIN Zhen-xi YOU Hui-guo LIU Yi HU Department of Respiratory and critical care Medicine Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Department of Respiratory and critical care Medicine The Central Hospital of Wuhan Tongji Medical College Huazhong University of Science and Technology Wuhan 430010 China

Atorvastatin is proven to ameliorate cardiac hypertrophy induced by chronic intermittent hypoxia （cIH）. However, little is known about the mechanism by which atorvastatin modulates cIH-induced cardiac hypertrophy, and whether specific hypertrophyrelated microRNAs are involved in the modulation. MiR-31 plays key roles in the development of cardiac hypertrophy induced by ischemia/hypoxia. This study examined whether miR-31 was involved in the protective role of atorvastatin against cIH-induced myocardial hypertrophy. H9c2 cells were subjected to 8-h intermittent hypoxia per day in the presence or absence of atorvastatin for 5 days. The size of cardiomyocytes, and the expression of caspase 3 and miR-31 were determined by Western blotting and RT-PcR, respectively. MiR-31 mimic or Ro 31-8220, a specific inhibitor of protein kinase c epsilon （PKcε）, was used to determine the role of miR-31 in the anti-hypertrophic effect of atorvastatin on cardiomyocytes. PKcε in the cardiomyocytes with miR-31 upregulation or downregulation was detected using RT-PcR and Western blotting. The results showed that cIH induced obvious enlargement of cardiomyocytes, which was paralleled with increased atrial natriuretic peptide （ANP）, brain natriuretic peptide （BNP）, and slow/beta cardiac myosin heavy-chain （MYHT） mRNA levels. All these changes were reversed by the treatment with atorvastatin. Meanwhile, miR-31 was increased by cIH in vitro. Of note, the atorvastatin pretreatment significantly increased the mRNA and protein expression of PKcε and decreased that of miR-31. Moreover, overexpression of miR-31 abolished the anti-hypertrophic effect of atorvastatin on cardiomyocytes. Upregulation and downregulation of miR-31 respectively decreased and increased the mRNA and protein expression of PKcε. These results suggest that atorvastatin provides the cardioprotective effects against cIH probably via up-regulating PKcε and down-regulating miR-31.

关键词： atorvastatin chronic intermittent hypoxia myocardial remodeling miR-31 protein kinase c epsilon

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丹参总酚酸对心肌缺血再灌注损伤保护作用的机制研究

丹参总酚酸对心肌缺血再灌注损伤保护作用的机制研究

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2012年中国药学大会暨第十二届中国药师周

作者：陈雯郭丽丽王阶中国中医科学院广安门医院心血管病证结合实验室

目的研究丹参总酚酸（TSA）对大鼠心肌缺血再灌注损伤的保护作用,阐明其作用机制。方法采用Langendorff离体心脏恒压灌流模型,30只雄性Wistar大鼠随机分为3组:空白对照组、I/R组及TSA组。空白对照组用K-H液持续灌注100min;I/R组（K-H液... 详细信息

目的研究丹参总酚酸（TSA）对大鼠心肌缺血再灌注损伤的保护作用,阐明其作用机制。方法采用Langendorff离体心脏恒压灌流模型,30只雄性Wistar大鼠随机分为3组:空白对照组、I/R组及TSA组。空白对照组用K-H液持续灌注100min;I/R组（K-H液灌流稳定20min后,停灌40min,复灌40min）;TSA组（复灌K-H液中含TSA0.2mg·mL-1,其他同I/R组）。动态检测心室内压,测定冠脉流量及心脏再灌流出液肌酸激酶（cK）含量变化,同时光镜下观察心肌细胞病理组织形态学变化,Western blotting法检测心肌匀浆、细胞胞浆及线粒体PKcε蛋白表达。结果与I/R组相比,TSA能明显改善缺血/再灌后的心功能,增加冠脉流量,减弱冠脉流出液中cK的活性（p＜0.05～0.01）,心肌细胞损伤程度减轻,增加心肌细胞PKcε蛋白表达,并促进PKcε由细胞质向线粒体的转位。结论 TSA对心肌I/R损伤具有明显保护作用,PKcε的激活及转位可能是TSA保护心肌细胞信号传导通路的组成部分。

关键词： myocardial reperfusion injury TSA protein kinase c epsilon

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