辛伐他汀抑制大鼠急性心肌梗死后心肌纤维化的实验研究

目的在大鼠结扎前降支致心肌梗死的模型上观察辛伐他汀抑制心肌纤维化的作用，探讨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，给予辛伐他汀干预。8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、IL-6表达量，并与假手术组比较。结果心肌梗死组（M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、IL-6表达升高（P〈0．01）。辛伐他汀干预组较M组辛RVWI、LVWI下降（P〈0．01），心肌中羟脯氨酸、胶原含量及IL-6表达下降（P〈0．01）。结论辛伐他汀减少急性心肌梗死后IL-6表达，抑制胶原形成及纤维化，可能是改善心室重塑和心功能的机制之一。

Experimental study of abating myocardial fibrosis after acute myocardium infarction by Simvastatin

Objective To investigate the effects of Simvastatin abating myocardial fibrosis after myocar-dium infarction and the possible mechanisms. Methods Simvastatin was given to the rats with myocardiac in-farction by left anterior decending coronary artery ligation. After 8 weeks, cardiac remodeling was observed through right ventricular weight index(RVWI) ,left ventrieular weight index(LVWI), The hydroproline(HC) and collagen content of two groups were recorded. The expression of IL-6 was detected. Results Compared with controls,the rat model of myocardiac infarction induced RVWI, LVWI increase(P < 0.01) ; The HC,collagen and IL-6 content rised(P < 0. 01). Simvastatin attenuated RVWI, LVWI(each P < 0.01) and decreased content of the HC, collagen and IL-6 (each P < 0. 01). Conclusion Simvastatin abate myocardial fibrosis, IL-6 and im-prove cardiac remodeling after acute myocardiac infarction.