目的 探讨瑞舒伐他汀对急性心肌梗死大鼠心肌组织蛋白表达的影响。方法 选取雌性健康SD大鼠,通过结扎左冠状动脉前降支建立急性心肌梗死模型54只,随机分为瑞舒伐他汀10、6 mg/kg组和模型组各18只,另选择18只作为假手术组。瑞舒伐他汀组根据临床常用剂量分别采用瑞舒伐他汀按照10、6 mg/kg剂量溶于蒸馏水中ig给药,模型组、假手术组均采用等量生理盐水ig给药,1次/d,持续4周。采用免疫组化法检测大鼠心肌组织中Periostin、调控机制核因子κB(NF-κB)、白细胞介素-6(IL-6)蛋白的表达差异,采用RT-PCR技术检测转化生长因子(TGF-β1)、Periostin、NF-κB及IL-6 的mRNA表达差异,比较各组大鼠的胶原容积分数(CVF)。结果 与模型组比较,瑞舒伐他汀10、6 mg/kg组大鼠Periostin蛋白灰度值以及NF-κB、IL-6蛋白阳性表达指数(PI)均显著下降(P < 0.05); Periostin、NF-κB、IL-6及TGF-β1 mRNA表达均显著下降(P < 0.05);CVF灰度值均显著下降(P < 0.05)。结论 瑞舒伐他汀可通过调节急性心肌梗死大鼠心肌组织中Periostin、NF-κB、IL-6、TGF-β1 mRNA及蛋白的表达来改善心肌重构。

Objective To investigate rosuvastatin on protein expression in myocardial tissue of rats with acute myocardial infarction (AMI). Methods Female SD rats were selected and established the rat model of AMI by ligation of the left anterior descending coronary artery (LAD). Fifty-four qualified rats were randomly divided into rosuvastatin groups with dosages of 10 & 6 mg/kg and the model group. And another 18 rats with Sham operations were selected into the control group. Rats in rosuvastatin groups were ig administered with rosuvastatin (adding into distilled water) with dosages of 10 and 6 mg/kg according to clinical common dosages, but the other Sham and model groups were ig administered with 0.9% saline solution. The treatment were adopted once daily, and lasted for 4 weeks. Protein expression difference of Periostin, nuclear factor κB (NF-κB), and interleukin -6 (IL-6) in myocardial tissue of rats were detected by immunohistochemistry method, expression of Periostin, NF-κB, IL-6, and TGF-β1 mRNA were detected by RT-PCR, and collagen volume fraction (CVF) of rats in each group were compared. Results Compared with model group, Periostin value and positive index (PI) of NF-κB, and IL-6 in rosuvastatin groups were obviously decreased (P < 0.05), and expressions of Periostin, NF-κB, IL-6, and TGF-β1 mRNA were obviously decreased (P < 0.05), and CVF value was also significantly reduced (P < 0.05). Conclusion Rosuvastatin can regulate protein expressions or mRNA expressions of Periostin, NF-κB, IL-6, and TGF-β1 to improve cardiac remodeling of rats with AMI.