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目的:观察瑞舒伐他汀对大鼠压力超负荷型心肌肥厚的作用,并探讨其对TGF-βl表达的影响。方法:将SD大鼠随机分为5组。除假手术组外各组通过不完全结扎大鼠腹主动脉构建心肌肥厚模型,A为假手术组,B为单纯手术组,C为卡托普利组(50mg/kgod),D组为瑞舒伐他汀小剂量组(2mg/kgod),E为瑞舒伐他汀大剂量组(4mg/kgod),各组动物术前一周始灌胃给予相应药物直至术后4周,A、B组给予等量生理盐水。给药第5周末,测定各组大鼠血压和心脏质量指数;采用RT-PCR法和免疫组化法检测左室心肌组织中TGF-βlmRNA和TGF-βl蛋白表达。结果:术后4周各组动物血压和HMI较A组明显增加(P<0.01或P<0.05),而C、D、E组较B组有显著下降(P<0.01或P<0.05);同时各治疗组左室心肌组织中TGF-βlmRNA和TGF-βl蛋白表达较B组有显著下降(P<0.01),且C组抑制表达较D、E组更为显著(P<0.05或P<0.01)。结论:瑞舒伐他汀可有效的缓解压力超负荷诱导的大鼠心肌肥厚,且作用类似卡托普利,其可能通过降低左室心肌TGF-βl表达,影响TGF-β信号转导产生作用。
Objective: To observe the effect of rosuvastatin on hypertensive cardiac hypertrophy in rats and its effect on the expression of TGF-β1. Methods: SD rats were randomly divided into 5 groups. In addition to the sham-operation group, the model of cardiac hypertrophy was established by incomplete ligation of the abdominal aorta in rats. A was sham-operated group, B was surgery alone, C was captopril (50mg / kgod), D (2mg / kgod), E was the high dose rosuvastatin group (4mg / kgod), and the animals in each group were given gavage for one week before operation until 4 weeks after operation, and the rats in groups A and B Equal amount of saline. At the end of the fifth week, the blood pressure and heart mass index of rats in each group were measured. The expressions of TGF-β1 mRNA and TGF-β1 protein in left ventricular myocardium were detected by RT-PCR and immunohistochemistry. Results: After 4 weeks, the blood pressure and HMI in each group were significantly increased (P <0.01 or P <0.05), while those in groups C, D and E were significantly lower than those in group B (P <0.01 or P <0.05). At the same time, the expression of TGF-β1 mRNA and TGF-β1 protein in left ventricular myocardium of each treatment group was significantly lower than that of B group (P <0.01), and the inhibition of C group was more significant than that of D and E groups (P <0.05 or P < 0.01). Conclusion: Rosuvastatin can effectively relieve cardiac hypertrophy induced by pressure overload in rats, and its effect is similar to that of captopril, which may affect TGF-β signal transduction by decreasing the expression of TGF-β1 in left ventricular myocardium.