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首页> 外文期刊>European review for medical and pharmacological sciences. >Atorvastatin improves cardiac function of rats with chronic cardiac failure via inhibiting Rac1/P47phox/P67phox-mediated ROS release
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Atorvastatin improves cardiac function of rats with chronic cardiac failure via inhibiting Rac1/P47phox/P67phox-mediated ROS release

机译:阿托伐他汀通过抑制Rac1 / P47phox / P67phox介导的ROS释放来改善慢性心力衰竭大鼠的心功能

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OBJECTIVE: To discuss the protective mechanisms of atorvastatin treatment for isoproterenol (ISO)-induced chronic heart failure. MATERIALS AND METHODS: The rats were randomly divided into three groups: normal group (n = 15, age-matched normal adult rats), ISO group (n = 11, ISO induced heart failure) and atorvastatin group (n = 14, ISO induced lesion but received atorvastatin treatment). The cardiac function was evaluated by echocardiography and hemodynamics analysis. In addition, the Rac1 activity in the myocardium and the expression levels of Rac1, p47phox and p67phox were measured by RT-PCR and western blot. RESULTS: Rats in ISO group developed into heart failure with decreased cardiac function. The Rac1, p47phox and p67phox mRNA expressions and ROS release were increased in ISO group. Atorvastatin treatment improved cardiac function of rats with isoproterenol-induced chronic heart failure and decreased the Rac1, p47phox and p67phox mRNA expressions. Also, membrane protein expression of Rac1 and ROS release decreased significantly. CONCLUSIONS: Atorvastatin may improve cardiac function of rats with heart failure via inhibiting Rac1/P47phox/P67phox-mediated ROS release.
机译:目的:探讨阿托伐他汀治疗对异丙肾上腺素(ISO)引起的慢性心力衰竭的保护机制。材料与方法:将大鼠随机分为三组:正常组(n = 15,年龄相匹配的正常成年大鼠),ISO组(n = 11,ISO诱发的心力衰竭)和阿托伐他汀组(n = 14,ISO诱发的)病变但接受了阿托伐他汀治疗)。通过超声心动图和血液动力学分析评估心功能。此外,通过RT-PCR和western blot检测心肌中Rac1的活性以及Rac1,p47phox和p67phox的表达水平。结果:ISO组大鼠发展为心力衰竭,心脏功能下降。 ISO组Rac1,p47phox和p67phox mRNA表达和ROS释放均升高。阿托伐他汀治疗改善了异丙肾上腺素诱发的慢性心力衰竭大鼠的心脏功能,并降低了Rac1,p47phox和p67phox mRNA表达。此外,Rac1和ROS释放的膜蛋白表达显着下降。结论:阿托伐他汀可能通过抑制Rac1 / P47phox / P67phox介导的ROS释放而改善心力衰竭大鼠的心功能。

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