蒙药顺气补心十一味丸对心肌梗死大鼠心肌血管生成和缺氧诱导因子1α表达的影响

Effects of Shunqi buxin shiyiwei pellet of Mongolian drug on myocardial angiogenesis and expression of HIF-1α in rats with myocardial infarction

目的:探讨蒙药顺气补心十一味丸对心肌梗死后缺血心肌血管生成和缺氧诱导因子1α(HIF-1α)表达的影响。方法:健康成年Wistar大鼠78只,随机分为正常对照组(6只)、模型对照组(18只)、蒙药低剂量组(18只)、蒙药高剂量组(18只)和卡托普利组(18只)。除正常对照组外所有大鼠背部皮下多点注射盐酸异丙肾上腺素(ISO)复制心肌梗死模型,模型建立后,蒙药低剂量组、蒙药高剂量组、卡托普利组分别在7d、28d和42d处死动物,观察CD34和HIF-1α蛋白的表达,以CD34阳性表达检测微血管密度(MVD)。结果:模型建立后7d、28d和42d,蒙药低、高剂量组与模型对照组相比MVD均明显增加(P均<0.01),卡托普利组在28d、42d时MVD较模型对照组显著增加(P均<0.01),与蒙药两组无显著差异;7d时HIF-1α表达在蒙药低(0.5610±0.0164)、高剂量组(0.5466±0.2135)较模型对照组(0.6060±0.0078)有显著增强(P<0.01),而卡托普利组(0.5892±0.0319)与模型对照组比较无显著差异;相应时间点各治疗组较模型对照组坏死灶面积缩小,42d时心肌纤维化程度减轻。结论:顺气补心十一味丸能够促进心肌梗死大鼠缺血心肌的血管生成,上调缺血心肌的缺氧诱导因子1α蛋白表达,其作用优于卡托普利。其促血管生成机制可能与上调缺血心肌的缺氧诱导因子1α蛋白表达有关。

Objective.. To explore effects of Shunqi buxin shiyiwei pellet （Mongolian drug） on angiogenesis of ische mic myocardium and expression of hypoxia-inducible factor-1α（HIF-1α） after myocardial infarction. Methods.. A total of 78 healthy adult Wistar rats were randomly divided into normal control group （n=6）, model control group （n= 18）, low dose Mongolian drug group （n= 18）, high dose Mongolian drug group （n= 18） and captopril group （n = 18）. Myocardial infarction models were established by subcutaneously multi-point injecting isoproterenol hydro- chloride （ISO） on back of rats. After establishment of model, rats of each group were executed on 7d, 28d and 42d, and expressions of CD34 and HIF-1α were observed. Microvessel density （MVD） was detected by positive expression of CD34. Results： Compared with model control group, MVD significantly increased in low and high dose Mongolian drug groups on 7d, 28d and 42d and in captopril group on 28d and 42d （P〈0.01 all）, MVD was no sig- nificant difference among two Mongolian drug groups and captopril group. Expressions of HIF-1α in low dose Mongolian drug group （0. 5610±0. 0164） and high dose Mongolian drug group （0. 5466±0. 2135） significantly in- creased compared with that of model control group （0. 6060±0. 0078） on 7d, P〈0.01, but there was no significant difference between captopril group （0. 5892 ± 0. 0319） and model control group. Compared with model control group, size of necrosis focus decreased and extent of myocardial fibrosis relieved on 42d in each therapy group. Conclusion： Shunqi Buxin Shiyiwei pellet can promote angiogenesis of ischemic myocardium and up-regulate expression of HIF-1α in rats with myocardial infarction. Its effect is more than that of captoprih Its mechanism of promotion of angiogenesis may be related with up-regulation of expression of HIF-1α in ischemic myocardium.