摘要
目的:研究解脲脲原体(Ureaplasma urealyticum,UU)能否诱导脐静脉内皮细胞(human umbilical vein endothelial cells,HUVEC)凋亡,并探讨其凋亡机制。方法:UU感染HUVEC 2、4、8、12 h后,用流式细胞术检测细胞凋亡率。并检测UU感染HUVEC 8 h后TNF-α、caspase-3及caspase-8产生量,同时检测加入TNF-α抗体、caspase-3和caspase-8抑制剂后的细胞凋亡率。结果:UU可以诱导HUVEC发生凋亡,与对照组差异有统计学意义(P<0.01);感染8 h后TNF-α、caspase-3、caspase-8的产生量均高于对照组(P<0.01);加入TNF-α抗体、caspase-3和caspase-8抑制剂后凋亡率均明显低于对照组(P<0.01)。结论:UU可以诱导HUVEC凋亡,并存在明显的时间效应关系,其凋亡机制可能是通过TNF-α介导的caspase-8及caspase-3激活的外源性死亡因子受体途径。
Objective：To study the occurence of apoptosis and the related mechanism of the human umbilical vein endothelial cells （HUVEC） induced by Ureaplasma urealyticum （UU）. Methods： The occurence of apoptosis of HUVEC was determined by flow cytometry at different times （2,4,8 and 12 h） after infected by UU. The productions of TNF-α,caspase-3 and caspase-8 in HUVEC after 8-hour infection of UU were detected by colorimetric assay, and the apoptosis rates were determined by flow eytometry when HUVEC was treated with TNF-α antibody, caspase-3 inhibitor or caspase-8 inhibitor prior to UU. Results： UU could induce the apoptosis occurrence of HUVEC with significant difference compared with control group. The productions of TNF-α, caspase-3 and caspase-8 were increased significantly in HUVEC infected by UU in contrast to control group, and the apoptosis occurence was significantly decreased when HUVEC was treated with TNF-α antibody, caspase-3 inhibitor or caspase-8 inhibitor. Conclusions ： The results suggested UU could induce the apoptosis occurrence of HUVEC with time-dependence. The mechanism was likely related to extrinsic death pathway dependent on TNF death receptor which induced caspase-8 and caspase-3 activations.
出处
《蚌埠医学院学报》
CAS
2010年第3期220-222,共3页
Journal of Bengbu Medical College
关键词
解脲脲原体
脐静脉
内皮细胞
凋亡
Ureaplasma urealyticum
umbilical vein
endothelial cells
apoptosis
