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目的:观察黄芪多糖(Astragalus polysaccharide,APS)对过氧化氢(H2O2)诱导的人脐静脉内皮细胞HUVECs损伤的保护作用及其可能的作用机制。方法:不同浓度的黄芪多糖孵育内皮细胞1h后加入400μmol/L的H2O2继续培养24h,用MTT法检测细胞活性;DAPI/PI双染法观察细胞形态并统计细胞凋亡率;硝酸还原酶法测定NO释放量;Western blot法测定Cu/Zn-SOD蛋白表达。结果:H2O2模型组细胞活性较之空白对照组下降42.87%,细胞核皱缩形态不规则化,细胞凋亡率升高了7倍、NO释放量降低42.96%,Cu/Zn-SOD蛋白表达下降45.31%;与模型组相比黄芪多糖各剂量组可不同程度改善这些变化,其中黄芪多糖1μg/ml组作用最为明显,其细胞活性和NO释放量分别增加24.96%、32.13%,细胞凋亡率降低36.02%,Cu/Zn-SOD蛋白表达升高37.14%。结论:黄芪多糖可能通过影响内皮细胞NO释放量和Cu/Zn-SOD蛋白表达,改善细胞NO与氧自由基的平衡发挥保护作用。
Objective: To observe the protective effect of Astragalus polysaccharide (APS) on hydrogen peroxide (H2O2) -induced HUVECs injury in human umbilical vein endothelial cells and its possible mechanism. Methods: HUVECs were incubated with different concentrations of APS for 1h and then cultured for 24h with 400μmol / L H2O2. Cell viability was measured by MTT assay. Morphological changes were observed by DAPI / PI double staining. Nitric acid reductase NO release; Western blot determination of Cu / Zn-SOD protein expression. Results: Compared with the blank control group, the cell viability in H2O2 group decreased by 42.87%, the cell nuclear shrinkage morphology was irregular, the apoptosis rate increased by 7 times, the NO release decreased by 42.96% and the expression of Cu / Zn-SOD protein decreased by 45.31 %. Compared with the model group, the APS groups could improve these changes to varying degrees. The most obvious effect was APS 1μg / ml group, the cell activity and NO release increased by 24.96% and 32.13%, respectively, and the apoptosis rate decreased 36.02%, Cu / Zn-SOD protein expression increased 37.14%. Conclusion: Astragalus polysaccharides may play a protective role by influencing NO release and Cu / Zn-SOD protein expression in endothelial cells and improving the balance between NO and oxygen free radicals.