DFMG对TNF-α诱导的人脐静脉内皮细胞CD40/CD40L相互作用的影响

The Effect of 7-Difluoromethoxy-5,4'-Dimethoxygenistein on CD40/CD40L Expression in HUVE-12 Cells Treated with Tumor Necrosis Factor-Alpha

目的:观察7-二氟甲氧基-5,4'-二甲氧基金雀异黄素(DFMG)对肿瘤坏死因子-α(TNF-α)诱导人脐静脉内皮细胞(HUVE-12)损伤模型的保护作用,探讨其保护作用的发挥是否与抑制CD40/CD40L相互作用相关。方法:体外培养人脐静脉内皮细胞(HUVE-12),20ng/mL TNF-α孵育诱导细胞损伤模型;加入不同浓度的DFMG,台盼蓝拒染法检测细胞活力、AnnexinⅤ-FITC/PI双染色流式细胞术检测细胞凋亡、流式细胞仪检测CD40/CD40L的表达。结果:DFMG呈浓度依赖性的升高TNF-α诱导的HUVEC-12细胞存活率;DFMG呈浓度依赖性的降低TNF-α诱导的HUVEC-12细胞凋亡;DFMG呈浓度依赖性降低CD40/CD40L表达。结论:DFMG保护TNF-α诱导的HUVEC-12细胞损伤,这种保护作用可能是通过抑制CD40/CD40L的表达发挥作用的。

Objective To examine if 7-difluoromethoxy-5,4'-dimethoxygenistein can protect Human umbilical vein endothelial cells from tumor necrosis factor-alpha injury through inhibiting CD40 / CD40L interaction. Methods HUVE-12 were cultured in vitro,20ng /mL TNF-α-induced cell injury model and treated with TNF-alpha and different concentrations of DFMG. The rate of cell viability is measured by using trypan blue staining,the apoptosis rate is detected by AnnexinⅤ-FITC / PI double staining flow cytometry and CD40 / CD40L expression was determined by flow cytometry. Results DFMG can increase the rate of cell viability in a concentration dependent manner. DFMG can significantly decrease the cell apoptosis rate in a concentration dependent manner. DFMG can significantly decrease CD40 / CD40L expression in a concentration dependent manner. Conclusion By inhibiting the expression of CD40 / CD40L,DFMG can antagonize TNF-α-induced inflammatory injury in HUVE-12 cells.