【摘要】 目的探讨二苯乙烯苷(TSG)如何保护TNF-α诱导的人脑微血管内皮细胞(HBMECs)损伤。方法体外培养HBMECs,然后用TNF-α分别诱导经TSG以及NF-κB抑制剂吡咯烷二硫氨基甲酸盐(PDTC)处理过的细胞,并检测细胞活力以及NF-κB p65和caspase-3的蛋白水平。结果 TNF-α能诱导HBMECs中NF-κB p65、caspase-3蛋白表达,而TSG则能抑制NF-κB p65、caspase-3的表达。相对于TNF-α单独处理组,用TSG或PDTC处理经TNF-α诱导的HBMECs细胞,能显著提高细胞活力,其机制是通过抑制NF-κB p65、caspase-3的蛋白表达从而起到保护作用。结论 TSG能够通过抑制NF-κB信号通路减轻TNF-α诱导的人脑微血管内皮细胞损伤。更多还原

【Abstract】 Objective This study aims to investigate how 2,3,5,4’-Tetrahydroxystilbene-2-O-β-D-glucoside(TSG) protects TNF-α induced human brain microvascular endothelial cells(HBMECs) damage mediated by N F-κB signaling pathway.Methods To test the effect of TSG or NF-κB inhibitor pyrrolidine dithiocarbamate(PDTC) on cell activity and NF-κB p65/caspase-3 expression,HBMECs were cultured in vitro and pretreated with different concentrations of TSG or PDTC before stimulation with TNF-α.Results Western-blot results showed that the expression of NF-κB p65 and caspase-3 increased significantly upon TNF-α stimulation,while the expression of which obviously decreased when treated with TSG.Compared to the group only stimulated by TNF-α,the cell activity of HBMECs clearly increased when treated with both TNF-α and TSG or PDTC.Interestingly,the cell activity of HBMECs was in a PDTC dose-dependent manner,which had significant difference in 80 and 160μmol/L group compared with that of TNF-α group(P < 0.05).Conclusion TSG is able to protect TNF-α-induced human brain microvascular endothelial cells damage by inhibiting NF-κB signaling.更多还原