连夏宁心方抑制心肌梗死后大鼠心室重构的作用及对促肾上腺皮质激素释放激素的影响

Study on inhibition of ventricular remodeling after myocardial infarction by Lianxia Ningxin Formula in rats and its influence on CRH

目的:验证网络药理学结果,并为连夏宁心方抑制心肌梗死后大鼠心室重构提供相关数据。方法:通过冠状动脉左前降支结扎诱导心肌梗死模型(n=6),连续干预4周后,观察大鼠的一般情况、体质量变化量、超声心动、血流动力学评估心室结构和心功能,HE染色观察心肌组织病理学改变,Western Blot检测下丘脑中促肾上腺皮质激素释放激素(CRH)蛋白的表达。结果:与空白组、假手术组比较,心梗组大鼠生活质量显著下降,且体质量增长最少;LVIDd、LVIDs、LVEDV、LVESV显著上升(P<0.01);+dp/dt max显著下降、LVEDP显著上升(P<0.01);CRH蛋白表达显著增高(P<0.01);连夏宁心方可显著改善上述情况。HE染色显示连夏宁心方组大鼠的心肌细胞变性较心梗组较少,排列较整齐,肌丝相对完整,间质相对均匀。结论:连夏宁心方能够抑制心肌梗死后大鼠心室重构和CRH的表达,一定程度上验证了网络药理学的结果。

Objective:To verify the results of network pharmacology and provide relevant data on ventricular remodeling in rats after Lianxia Ningxin Formula(LXNX)inhibited myocardial infarction.Methods:The myocardial infarction model(n=6)was induced by ligation of the left anterior descending coronary artery.After continuous intervention for 4 weeks,the general condition,body weight change,echocardiography and hemodynamics of the rats were observed to evaluate the ventricular structure and cardiac function.The pathological changes of myocardial tissue were observed by HE staining,and the expression of CRH protein in the hypothalamus was detected by Western Blot.Results:Compared with the control group and sham group,the quality of life of the rats in the model group was significantly reduced,and the change of body weight was the least,LVIDd,LVIDs,LVEDV and LVESV were significantly increased(P<0.01),+dp/dt max was significantly decreased(P<0.01),LVEDP was significantly increased(P<0.01),CRH expression was significantly increased(P<0.01),LXNX formula could significantly improve the above situation.HE staining showed that the degeneration of myocardial cells in LXNX group was less than that in model group,the arrangement was more neater,the myofilament was relatively complete,and the stroma was relatively uniform.Conclusion:LXNX formula can inhibit ventricular remodeling and CRH expression in rats after myocardial infarction,which verifies the results of network pharmacology to a certain extent.