摘要
目的在大鼠结扎前降支致心肌梗死的模型上观察氯沙坦和辛伐他汀抑制心肌纤维化的作用,初步探讨氯沙坦和辛伐他汀改善心室重塑和心功能的机制。方法结扎大鼠冠状动脉前降支造成心肌梗死模型,给予氯沙坦和辛伐他汀干预。4周后,测定心脏重量指数、心肌梗死区与非梗死区心肌羟脯氨酸含量和胶原含量,检测不同分组的大鼠心肌中MMP-1、IL-6和IL-10水平差异,并与假手术组比较。结果心肌梗死组(MI组)大鼠右室重量指数(RVWI)、左室重量指数(LVWI)升高(P<0.01)。心肌中羟脯氨酸、胶原含量、MMP-1、IL-6和IL-10表达升高(P<0.01)。氯沙坦和辛伐他汀干预组较MI组RVWI、LVWI下降(P<0.01),心肌中羟脯氨酸、胶原含量及MMP-1、IL-6和IL-10表达下降(P<0.01);尤其以氯沙坦联合辛伐他汀干预组下降更明显。结论氯沙坦联合辛伐他汀减少急性心肌梗死后炎性因子及基质金属蛋白酶表达,抑制胶原形成及纤维化,可能是改善心室重塑的机制之一。
Objective To investigate the effect of anterior descending artery ligation in rats induced by myocardial infarction model of Losartan and Simvastatin inhibited the role of myocardial fibrosis, and to study the mechanism of losartan and simvastatin on ventricular remodeling and cardiac function. Methods Simvastatin was given to the rats with myocardial infarction by left anterior descending coronary artery ligation. After 8 weeks, cardiac remodeling was observed through right ventricular weight index （RVWI）, left ventricular weight index （LVWI）, The hydroproline （HC） and collagen content of five groups were recorded. The expression of MMP-1, IL-6 and IL-10 was detected. Results Compared with controls, the rat model of myocardial infarction induced RVWI, LVWI increase （P〈0.01）; The HC, collagen and MMP-1, IL-6 and IL-10 content rised （P〈0.01）. Simvastatin and Losartan attenuated RVWI, LVWI （each P〈0.01） and decreased content of the HC, collagen and MMP-1, IL-6 and IL-10 （each P〈0.01）. Conclusion Simvastatin and Losartan abate the expression of MMP-1, IL-6 and IL-10 and improve cardiac remodeling after acute myocardial infarction.
出处
《中国医药指南》
2009年第22期13-15,共3页
Guide of China Medicine
