目的 研究丹酚酸B促进缺血心肌血管生成的分子作用机制。方法 制备心肌梗死大鼠模型，50只大鼠随机分为假手术组、模型组及丹酚酸B低、中、高（20、40、60 mg/kg）剂量组，尾iv给药1周后，测定大鼠心肌梗死面积；免疫组化法检测大鼠心肌梗死边缘区微血管密度；试剂盒检测大鼠血清中肌酸激酶同工酶MB（CK-MB）、心肌肌钙蛋白（cTnI）和乳酸脱氢酶（LDH）的量；Western blotting法检测大鼠心肌梗死边缘区核转录因子E2相关因子2（Nrf2）、血红素加氧酶（HO-1）、血管内皮生长因子（VEGF）蛋白的表达水平。结果 与模型组比较，丹酚酸B中、高剂量组大鼠心肌梗死面积显著减少（P<0.05）；丹酚酸B低、中、高剂量组大鼠微血管密度显著增加（P<0.05）；丹酚酸B中、高剂量组大鼠血清CK-MB、LDH和cTnI水平显著下降（P<0.05）；丹酚酸B低、中、高剂量均可增加大鼠心肌梗死边缘区VEGF、Nrf2和HO-1蛋白水平的表达（P<0.05），其中以丹酚酸B高剂量组效果最佳。结论 丹酚酸B可促进大鼠缺血心肌血管再生，该作用与其增加心肌组织VEGF、Nrf2和HO-1的表达有关。

Objective To investigate the molecular mechanism of salvianolic acid B (Sal B) in the angiogenesis in rats with myocardial ischemia (MI). Methods The acute ischemia model was established. The rats were divided randomly into the sham operation group, model group, and Sal B treatment (20, 40, and 60 mg/kg) groups. The drugs were tail administration for 1 week. The microvascular density (MVD) in the marginal zone of myocardial infarction of rats were determinated, the levels of CK-MB, cTnI, and LDH were detected by kits, and the expression of myocardial VEGF, Nrf2, and HO-1 were examined by Western blotting. Results Compared with the model group, the infarct area was reduced obviously in Sal B 40 mg/kg group and 60 mg/kg group in MI rats (P < 0.05). And Sal B (20, 40, and 60 mg/kg) resulted in an obvious increase in MVD of MI rat (P < 0.05). Compared with the model group, the levels of CK-MB, LDH, and cTnI of medium and high dose groups were significantly decreased (P < 0.05). In addition, Sal B of 20, 40, and 60 mg/kg could increase the expression of VEGF, Nrf2, and HO-1 protein levels (P < 0.05). And that Sal B 60 mg/kg led to strong expression of above proteins.Conclusion Sal B induces angiogenesis in rats after MI. The role of Sal B on angiogenesis is correlated with the increased expression of VEGF, Nrf2, and HO-1 in the myocardium.

西安市科技计划项目（2017121SF/YX015）