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观察黄芪多糖(APS)对人微血管内皮细胞(HMEC-1)的保护作用以及Akt通路其中发挥的角色,以期探索APS细胞保护作用机制。用MTT法考察APS对HMEC-1细胞活力的影响;用体外缺氧缺糖(oxy-gen-glucose deprivation,OGD)模型,在OGD条件下,用LDH法检测细胞死亡率;用Western blotting法,研究APS对Akt通路的调节作用;利用Akt抑制剂Wortmannin作为阻断剂,考察Akt通路在APS细胞保护作用中发挥的角色。结果表明APS对HMEC-1细胞活力无明显影响,对OGD诱导的内皮细胞死亡具有一定的保护作用,可以显著减少细胞死亡率,且其保护作用具有剂量依赖性。且APS能诱导Akt磷酸化,而Akt抑制剂Wortmannin可降低APS对OGD诱导的内皮细胞死亡的保护作用。这些结果提示,APS可能是通过诱导Akt磷酸化,保护细胞减少OGD诱导的细胞死亡。
To observe the protective effect of astragalus polysaccharides (APS) on human microvascular endothelial cells (HMEC-1) and the role of Akt pathway in exploring the protective mechanism of APS. The effect of APS on the viability of HMEC-1 cells was examined by MTT assay. The cell death rate was detected by LDH assay using OGD model in vitro. To study the regulatory effect of APS on Akt pathway; use Akt inhibitor Wortmannin as a blocker to investigate the role of Akt pathway in the protection of APS cells. The results showed that APS had no significant effect on the viability of HMEC-1 cells and had a protective effect on OGD-induced endothelial cell death, which could significantly reduce the cell death rate and its protective effect in a dose-dependent manner. And APS can induce Akt phosphorylation, while Akt inhibitor Wortmannin can reduce the protective effect of APS on OGD-induced endothelial cell death. These results suggest that APS may protect cells from OGD-induced cell death by inducing Akt phosphorylation.