益气逐瘀方对急性心肌梗死大鼠miR-24表达及心肌细胞凋亡的影响

目的:观察益气逐瘀方参元丹对急性心肌梗死大鼠miR-24表达及心肌细胞凋亡的影响。方法:50只SD大鼠随机分为假手术组、模型组、参元丹高、中、低剂量组,每组10只,采用左冠状动脉前降支结扎法复制心肌梗死模型,参元丹高、中、低剂量组从术后第2天开始给予参元丹药液灌胃,假手术组和模型组给予等剂量生理盐水灌胃,共给药2周。治疗结束后检测大鼠血清CK、LDH水平及心肌组织miR-24基因表达情况,TUNEL法检测心肌细胞凋亡。结果:实验结束时,与模型组相比,参元丹高、中、低剂量组均能显著降低血清CK、LDH水平(P0.05,P0.01),升高心肌组织miR-24 mRNA表达(P0.05,P0.01),同时降低心肌细胞凋亡指数(P0.05,P0.01)。结论:益气逐瘀方参元丹能够减轻心肌梗死大鼠心肌损伤及细胞凋亡,其作用机制可能与上调心梗大鼠缺血心肌组织miR-24基因表达有关。

Effects of Shen Yuan Dan on MIR-24 Expression and Myocardium Cell Apoptosis in Myocardial Infarction Rats

To observe the effects of Shen Yuan Dan(SYD) on MIR-24 expression and myocardium cell apoptosis in myocardial infarction rats. Methods: Fifty SD rats were randomly divided into five groups, namely sham group, model group, high dose, middle dose, and low-dose SYD group, with 10 rats in each group. The myocardium ischemia models were established by ligating of anterior descending branch of coronary artery. The rats in treatment groups were treated with intragastric administration of SYD. The model and sham group were given 0.9% sodium chloride solution with the same volume. The treatment lasted for 2 weeks. Serum levels of creatine kinases (CK), lactate dehydrogenase (LDH) and MIR-24 gene expression in ischemic myocardium were measured after the treatment. Myocardial apoptosis was measured by TUNEL. Results: At the end of the treatment, the serum level of CK and LDH significantly decreased in SYD (high, middle and low-dose) groups compared with those of the model group (P<0.05, P<0.01). And the MIR-24 mRNA expression in ischemic myocardium were significantly increased in SYD (high and middle-dose) groups compared with those of model group (P<0.05, P<0.01). Meanwhile, the myocardial apoptosis index also significantly decreased in STD groups (high, middle, and low-dose) compared with those in model group (P<0.05, P<0.01). Conclusion: Yiqi Zhuyu formula SYD could relieve myocardial injury and cell apoptosis in myocardium infarction rats. The possible mechanism may relate to up regulating MIR-24 gene expression in ischemic myocardium.