摘要
目的:探讨辛伐他汀对大鼠心肌梗死(MI)后心室重构的作用及对心肌Smad7表达的影响。方法:建立大鼠MI模型,24h后存活大鼠随机分成MI组(n=9)、辛伐他汀20mg组(20mg·kg-1·d-1,Sim2组,n=10)和40mg组(40mg·kg-1·d-1,Sim4组,n=9),另设假手术组(Sham组,n=10)。4周后观察血脂水平、心室重量指数、天狼猩红染色分析左室非梗死区胶原容积分数、苏木精-伊红染色及电镜观察心肌组织病理改变,并用免疫组化染色和RT-PCR检测Smad7在非梗死区的表达。结果:各组血脂水平差异无统计学意义,MI组左心室重量指数增加,非梗死区Ⅰ型、Ⅲ型胶原容积分数及Ⅰ/Ⅲ比值均增加。与MI组相比,Sim组左室重量指数降低,非梗死区Ⅰ型、Ⅲ型胶原容积分数及Ⅰ/Ⅲ比值下降,但仍高于Sham组,心肌组织病理结构改善。与MI组比较,Sim组Smad7表达增加。结论:辛伐他汀能有效地减轻MI后的心肌损伤和纤维化重构,其机制与其调脂作用无关,可能与促进Smad7的表达有关。
Objective： To assess the elects of simvastatin on ventricular remodeling in rats after myocardial infarction and to investigate the alternation of the expression of smad7 on myocardium. Method： Twenty-four hours after myocardial infarction by left anterior descending coronary artery ligation, the survival rats were randomly di- vided into myocardial infarctiongroup（MI, n=9）, simvastatin20 mg·kg^-1·d^-1 treatment group（Sire2, n=10） and simvastatin 40 mg·kg^-1·d^-1 treatment group（Sim4, n=9）. Sham-operated animals underwent identical surgery except for the coronary artery ligation（Sham, n= 10）. After 4 weeks, the effects of sinvastatin on myocardial fibrosis were evaluated by detecting changes of left ventrieular weight index（LVWI）, the collagen volume fraction（CVF） in non infarction zone（NIZ） with Picric-Sirius Red Polarimetry, and the expressions of Smad7 in NIZ by immunohistochemical staining and reverse transcription poiymerase chain reaetion（RT-PCR）. The myocardial histopathology was also examined by HE staining and an electron microscope. At the same time, levels of set urn lipids were measured. Result：There were no significant differences in all groups in levels of serum lipids（P〉 0.05）. Comparing with Sham group, LVWI , the typeⅠ CVF, type Ⅲ CVF and the Ⅰ/Ⅲ ratio in NIZ were in creased significantly in MI group. Comparing with MI group, the LVWI, the type Ⅰ CVF and type Ⅲ CVF in NIZ and the Ⅰ /Ⅲ ratio were decreased significantly in Sire groups, but higher than those in Sham group. Corn pared with MI groups, the histological changes of fibrosis and the ultrastructural alterations in rats treated with simvastatin were also obviously improved. Contrasted to MI group, the expressions of Smad7 were significantly increased in Sim groups. Conclusion： simvastatin has a protective effect on myocardial injury and can ameliorate myocardial fibrosis in rats induced by Mh The mechanisms of simvastatin anti fibrosis could be independent of its lipid-lower
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2009年第6期445-448,共4页
Journal of Clinical Cardiology
基金
重庆市自然科学基金资助项目(渝科发计字[2004]54号文)
