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目的观察芪苈强心胶囊对慢性心力衰竭(CHF)大鼠心室重构的影响及机制。方法 Wistar大鼠200只,采用结扎大鼠冠状动脉左前降支的方法造成心肌梗死,8周后形成CHF大鼠模型,随机分为模型组(予蒸馏水)、假手术组(予蒸馏水)、芪苈强心胶囊高剂量组(1.0g/kg)、中剂量组(0.5g/kg)、低剂量组(0.25g/kg)、缬沙坦组(20mg/kg),每组7只。连续给药4周后,RT-PCR法测定CHF大鼠心肌组织中配体门控型嘌呤受体(P2X1～P2X7)mRNA的表达水平。结果与假手术组比较,模型组大鼠心肌组织中P2X2、P2X4、P2X5、P2X6受体亚型mRNA水平显著降低(P<0.05或P<0.01);与模型组比较,芪苈强心胶囊高剂量组能上调P2X2、P2X4、P2X5、P2X6等受体亚型mRNA水平(P<0.05);与假手术组比较,模型组大鼠心肌组织中P2X3受体亚型mRNA水平显著升高(P<0.05),但各给药组与模型组比较差异均无统计学意义(P>0.05)。结论芪苈强心胶囊可调节CHF大鼠心肌组织的P2X受体mRNA表达水平,从而改善心室收缩功能,增加心输出量,抑制心力衰竭的心室重构的作用机制可能与上调P2X2、P2X4、P2X5、P2X6受体mRNA表达有关。
Objective To observe the effect of Qili Qiangxin Capsule on ventricular remodeling in chronic heart failure (CHF) rats and its mechanism. Methods 200 Wistar rats were inflicted with myocardial infarction by ligation of the left anterior descending coronary artery. After 8 weeks, CHF rats were randomly divided into model group (pre-distilled water), sham operation group (pre-distilled water) Qiangqiang capsule high dose group (1.0g / kg), middle dose group (0.5g / kg), low dose group (0.25g / kg), valsartan group (20mg / kg) Four weeks after continuous administration, the expression of ligand-gated P2X1-P2X7 mRNA in myocardium of CHF rats was determined by RT-PCR. Results Compared with the sham operation group, the mRNA levels of P2X2, P2X4, P2X5 and P2X6 receptor subtypes in the model group were significantly decreased (P <0.05 or P <0.01). Compared with the model group, Compared with sham operation group, P2X2, P2X4, P2X5, P2X6 and other receptor subtypes mRNA levels were increased in the dose group (P <0.05). Compared with the sham operation group, the mRNA level of P2X3 receptor subtype in the model group was significantly increased (P < 0.05), but there was no significant difference between each administration group and the model group (P> 0.05). Conclusion Qili Qiangxin Capsule can regulate the expression of P2X receptor mRNA in the myocardium of CHF rats, so as to improve the ventricular systolic function, increase the cardiac output and inhibit the ventricular remodeling in heart failure. The mechanism may be related to the up-regulation of P2X2, P2X4, P2X5 , P2X6 receptor mRNA expression.