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作 者:张莹[1] 王安才[1] 王新[1] 王德国[1] 邢文[1]
出 处:《中国临床药理学与治疗学》2016年第9期968-972,共5页Chinese Journal of Clinical Pharmacology and Therapeutics
基 金:国家自然科学基金(81200142)
摘 要:目的:观察压力高血压大鼠心肌组织蛋白酶S、K(Cat S、Cat K)的表达,并探讨阿托伐他汀对肥厚心肌的逆转作用和机制。方法:将雄性SD大鼠45只随机分配到假手术组、模型组和阿托伐他汀组,模型组及阿托伐他汀组通过不完全结扎大鼠腹主动脉的手术方法构建心肌肥厚模型,采用RT-PCR方法和免疫组化的方法分别检测心肌Cat S、Cat K mRNA及蛋白表达,用Masson染色法分析左心室肌质量。结果:模型组及阿托伐他汀组左室重量指数、心肌Cat S、Cat K mRNA及蛋白表达较假手术组均明显升高(P<0.05),但阿托伐他汀组较模型组显著降低(P<0.05)。结论:阿托伐他汀可有效地改善压力超负荷诱导的大鼠心肌肥厚,其机制可能系通过下调心肌Cat S、Cat K表达所产生。AIM: To observe the expression of Cat S,Cat K in myocardium of the rats with pressure-overloaded cardiac hypertrophy and explore the mechanisms of atorvastatin on reversing cardiac hypertrophy. METHODS: Forty-five SD rats were randomly divided into 3 groups: sham group,model group and atorvastatin group. All groups were undertaken the incomplete constriction of the abdominal aorta to form the myocardium hypertrophic models except the sham group. The weight of rats and left ventriculium were calculated for the left ventricular weight index. The expression of Cat S,Cat K mRNA and protein were detected by RT-PCR and immunohistochemi respectively. Masson 's was used to analysis the fibrosis of the left ventricle muscle. RESULTS: The left ventricular weight index in model group and atorvastatin group were significantly higher than that in sham group( P〈0. 05). The myocardial Cat S,Cat K mRNA expression of the model group and atorvastatin group were also increased significantly( P〈0. 05). But the myocardial Cat S,Cat K mRNA and protein expression of atorvastatin group were lower than that in model group( P〈0. 05). CONCLUSION: Atorvastatin can effectively ameliorate the myocardial hypertrophy from pressure overload,which may be related to decrease the expression of Cat S,Cat K in myocardium.
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