目的研究川芎嗪与黄芪甲苷配伍对缺氧诱导损伤的人脐静脉内皮细胞(HUVECs)的增殖的影响及机制。方法建立HUVECs缺氧损伤模型,将细胞分为5组,对照组、模型组、川芎嗪(80μg/mL)组、黄芪甲苷(40μg/mL)组及川芎嗪(80μg/mL)+黄芪甲苷(40μg/mL)组,MTT法检测川芎嗪、黄芪甲苷及其配伍对缺氧损伤HUVECs增殖的影响;免疫组化法检测缺氧损伤HUVECs细胞VEGF、Ang-II蛋白表达,Western blotting检测VEGF和Ang-II蛋白的表达,RT-PCR检测VEGF和Ang-II mR NA表达。结果与模型组相比,川芎嗪与黄芪甲苷均能提高细胞存活率,川芎嗪与黄芪甲苷配伍组具有极显著差异(P<0.001);川芎嗪与黄芪甲苷配伍提高VEGF、Ang-II蛋白表达。同时,川芎嗪与黄芪甲苷配伍组能上调VEGF和Ang-II mR NA的表达(P<0.001)。结论川芎嗪与黄芪甲苷配伍可能通过增加血管生成靶向因子VEGF和Ang-II的表达发挥促进血管生成的作用。 Objective To investigate the effects of ligustrazine and astragaloside on the proliferation of hypoxia-induced human umbilical vein endothelial cells (HUVECs) and its mechanism. Methods HUVECs were induced by hypoxia. The cells were divided into 5 groups: control group, model group, ligustrazine 80μg / mL, Astragaloside 40μg / mL and ligustrazine 80mg / (40μg / mL). MTT assay was used to detect the effects of ligustrazine, astragaloside and its compatibility on the proliferation of HUVECs induced by hypoxia. The expressions of VEGF and Ang-II protein in HUVECs were detected by immunohistochemistry and Western blotting VEGF and Ang-II protein expression, RT-PCR detection of VEGF and Ang-II mR NA expression. Results Compared with the model group, ligustrazine and astragaloside could increase the cell viability. The combination of ligustrazine and astragaloside had significant difference (P <0.001), and the combination of ligustrazine and astragaloside increased the expression of VEGF and Ang- II protein expression. At the same time, the combination of ligustrazine and astragaloside could upregulate the expression of VEGF and Ang-II mR NA (P <0.001). Conclusion The combination of ligustrazine and astragaloside IV may play an important role in promoting angiogenesis by increasing the expression of VEGF and Ang-II.