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目的探讨丹参酮ⅡA促血管生成的作用机制。方法将人脐静脉内皮细胞系(HUV-EC-C)分为空白组、二甲基亚枫(DMSO,终浓度1%)组、血管内皮生长因子(VEGF,终浓度5μg/L)组、丹参酮ⅡA(终浓度6mg/L)组,分别加入相应药物48h后,镜下观察各组细胞形态,并采用蛋白质印迹法测定各组细胞内皮型一氧化氮合酶(eNOS)、磷酯酰肌醇-3激酶(PI3K)表达情况。结果 VEGF组和丹参酮ⅡA组HUV-EC-C细胞形态饱满,丰度明显增加,细胞间隙缩小,均未见脱落。与空白组比较,VEGF组和丹参酮ⅡA组细胞eNOS、PI3K蛋白表达均显著增强(P<0.05或P<0.05)。结论丹参酮ⅡA能提高HUV-EC-C内PI3K和eNOS蛋白表达,可能是其促血管生成的作用机制之一。
Objective To explore the mechanism of Tanshinone ⅡA promoting angiogenesis. Methods Human umbilical vein endothelial cell line (HUV-EC-C) was divided into blank group, DMSO group (1% DMSO), vascular endothelial growth factor (VEGF) Tanshinone IIA (final concentration 6mg / L) were added into the corresponding drugs for 48h. The morphological changes of the cells were observed under light microscopy. The expressions of eNOS and phosphatidylinositol Alcohol-3 kinase (PI3K) expression. Results The HUV-EC-C cells in VEGF group and TanshinoneⅡA group were full and abundant, their abundance was significantly increased, and the cell gap was reduced. Compared with the blank group, the expressions of eNOS and PI3K in VEGF and Tanshinone ⅡA groups were significantly increased (P <0.05 or P <0.05). Conclusion Tanshinone Ⅱ A can increase the protein expression of PI3K and eNOS in HUVECs, which may be one of the mechanisms of angiogenesis.