二苯乙烯苷对氧化损伤人脐静脉内皮细胞NF-κB表达的影响

Effect of TSG on H_2O_2 Induced NF-κB Expression in Human Umbilical Vein Endothelial Cells

目的研究二苯乙烯苷(TSG)对过氧化氢诱导人脐静脉内皮细胞损伤的保护作用,并探讨其作用机制。方法以不同浓度(0.1、1.0和10.0μmol/L)的二苯乙烯苷孵育体外培养人脐静脉内皮细胞4 h后,用200μmol/L过氧化氢作用内皮细胞24 h,采用电镜观察、MTT等方法测定各组细胞活力;RT-PCR、Western-blot检测基因NF-κB、IκB表达。结果与对照组比较,不同剂量组TSG均可以提高过氧化氢诱导损伤的人脐静脉内皮细胞活性,降低NF-κB mRNA及蛋白水平的表达,其中以1μmol/L TSG组的作用最明显(P<0.01),但对IκB基因表达的影响差异均无显著性(P>0.05)。结论二苯乙烯苷对氧化损伤的人脐静脉内皮细胞具有抗氧化保护作用,其作用机制可能与下调NF-κB的表达、阻断细胞NF-κB/IκB信号通路有关。

Objective To study the protective effect of TSG on human umbilical vein endothelial cells（hUVECs） injury induced by H2O2 and explore the related mechanism of action.Methods HUVEC treated with TSG（0.1,1.0,10.0 μmol/L） for 4 hours then exposed to 200 μmol/L H2O2 for 24 hours.Cell viability was determined by electron microscope observation and MTT assay.Gene expression of NF-κB and IκB were measured by RT-PCR and Western-blot. Results Compared with the model group,the cell viability of hUVEC impaired by H2O2 can be protected by different concentrations of TSG,especially by 1 μmol/L TSG treated groups.The expression of NF-κB mRNA and protein remarkably decrease（P0.01）,and there were no effect for the expression of IκB. Conclusion TSG have a protective effect on the hUVECs impairment induced by H2O2,and the potential mechanism of action may be associated with downregulating the expression of NF-κB and blocking NF-κB/IκB signal pathway.