Objective To investigate the effect of captopnl on ventncular remadeling and cardiac function and the expresrnsion tumor necrosis factor-alpha( TNF-α ) and matrix metalloproteinase-2 ( MMP-2 ) in rats with myocardial infarction. Methods rnMyocardial infarction model was established by ligation of the anterior descending coronary artery in rats. After 24 hours of operarntion, survival rats were randomly divided into model group, model + captopril group ( rats were treated with 500 mg · kg -1 · d - 1 caprntopril in their drinking water),twelve rats in each group. Six rats were selected randomly without ligation as sham operation rngroup. The sham operation group and model group were treated with water. Six weeks after operation , TNF-α and type Ⅰ and rnⅢ collagen were detected with immunohistochemistry; MMP-2 protein were detected by westem-blot; Collagen volume fraction rn( CVF) was assessed with Van Gieson. Left ventricular haemodynamics changes were recorded with baroceptor. Results Comrnpared with sham operation group, the left ventricular function of rats in model group and model + captopril group were obvirnously degraded( P ＜ 0. 05 ) ; Captopril could significantly improve ventricular function after myocardial infarction ( P ＜ 0. 05 ) .rnCVF and type Ⅰ /Ⅲ collagen ratio of non-infarct zone in model group and model + captopril group were significantly higher rnthan those in sham operation group( P ＜ 0. 01 ) ;Total hean weight/ body weight ( THW/BW) and left ventricular weight / body rnweight ( LVW/BW) obviously increased ( P ＜0. 01) . But the CVF, type Ⅰ/Ⅲ collagen ratio, THW/BW and LVW/BW in rnmodel + captopril group were significantly lower than those in the model group( P ＜ 0. 05 ) . The expression of TNF-α and MMPrn2 in the non-infarcted zone of model group were significantly higher than those in sham operation group ( P ＜0. 01) ; But in model + captopril group, the expression of TNF-α and MMP-2 were decresed compared with model group (P ＜0. 01). Conrndusion Captopril could lessen the left ventricular remodeling after myocardial infarction in rats and improves cardiac funcrntion. These effects could be relevant to regulate the expression of MMP-2 and TNF-α.%目的 探讨卡托普利对心肌梗死后心力衰竭大鼠心肌肿瘤坏死因子-α(TNF-α)、基质金属蛋白酶-2(MMP-2)的表达以及心室重构和心室功能的影响.方法 结扎大鼠冠状动脉前降支建立心肌梗死模型,术后24 h存活大鼠分为模型组和模型+卡托普利组(卡托普利500 mg·kg-1·d-1,饮水给药).另设假手术组,假手术组和模型组大鼠饲普通饮水.术后6周免疫组织化学法检测TNF-α、Ⅰ型和Ⅲ型胶原,蛋白印迹法检测MMP-2,Van Gieson染色测胶原容积分数;压力传感器记录左心室血流动力学改变.结果 与假手术组相比,模型组和模型+卡托普利组大鼠的心室功能明显降低(P<0.05),卡托普利能显著改善心肌梗死后心室功能(P<0.05);与假手术组相比,模型组和模型+卡托普利组非梗死区胶原容积分数(CVF)、Ⅰ/Ⅲ胶原比均升高(P<0.01),全心质量/体质量(THW/BW)及左心室实际质量/体质量(LVW/BW)显著增加(P<0.01);但卡托普利干预后CVF、Ⅰ/Ⅲ胶原比及THW/BW、LNW/BW均低于模型组(P<0.05).与假手术组相比,模型组非梗死区MMP-2和TNF-α表达升高(P<0.01);卡托普利干预后MMf-2和TNF-α的表达明显低于模型组(P<0.01).结论 卡托普利能明显减轻大鼠心肌梗死后心室重构,改善心室功能,其作用可能与调节心脏TNI-α和MMP-2的表达有关.
展开▼
