冠心Ⅴ号合剂干预急性心肌梗死模型大鼠心室重构及心肌TLR4信号通路研究

Guanxin V Mixture Intervention on the Ventricular Remodeling and Myocardial TLR4 Signal Pathway in Rat Model of Acute Myocardial Infarction

目的:观察冠心Ⅴ号合剂对急性心肌梗死(AMI)模型大鼠心室重构及心肌TLR4信号通路的影响。方法:雄性SD大鼠56只,采用冠状动脉左前降支结扎法建立急性心肌梗死模型,分别给予冠心Ⅴ号合剂小剂量(0.5 g/ml)、中剂量(1 g/ml)、大剂量(2 g/ml)及血脂康胶囊连续干预4周,以心脏彩超观察心脏结构及心功能,荧光定量PCR法检测TLR4mRNA、Myd88mRNA、NF-κBmRNA表达。结果:模型组实验大鼠心功能明显下降,梗死区心肌组织TLR4mRNA、Myd88mRNA、NF-κBmRNA表达上调,与空白组、假手术组比较差异有统计学意义;药物干预组各组上述指标均低于模型组;冠心Ⅴ号合剂大剂量组上述指标低于余治疗组,差异有统计学意义。结论:冠心Ⅴ号合剂能够抑制急性心肌梗死大鼠TLR4信号通路并改善心室重构。

Objective：Observing the effect of Guanxin V mixture on ventricular remodeling and TLR4 signaling pathway in myocardial Tissue in rats with acute myocardial infarction. Methods： 56 male SD rats, establishing the model of acute myocardial infarction by left anterior descending coronary artery ligation. All of them were treated with low Guanxin V mixture dose（0. 5 g/ml） ,medium dose（ 1 g/ml）, high dose（ 1 g/ml） and Xuezhikang Capsule for 4 weeks,To observe the cardiac structure and function by echocardiography, Fluorescence quantitative PCR technique was used to detect the expression of TLR4mRNA, Myd88mRNA, NF-KBmRNA. Result： Compared with the normal group and sham operation group,the expression of TLR4mRNA, Myd88mRNA, NF-KBmRNA in model rats were up-regulation,the difference were statistically significant, Drug intervention group were lower than those in the model group, the difference were statistically significant. The mRNA expression of Guanxin V mixture groups are proportional to the concentration of each drug, the difference was statistically significant. Conclusion： Guanxin V mixture can inhibit TLR4 signal pathway, and improve ventricular remodeling.