摘要
目的了解金黄色葡萄球菌(金葡菌)α溶血素诱导脐静脉内皮细胞凋亡机制。方法将不同浓度金葡菌α溶血素感染脐静脉内皮细胞8h后,检测TNF-α、caspase-3及caspase-8的产生量,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。结果金葡菌α溶血素感染脐静脉内皮细胞8h后,TNF-α、caspase-3、caspase-8的产生量与对照组相比差异有统计学意义(P<0.01);而加入TNF-α抗体、caspase-3和caspase-8抑制剂后凋亡率明显降低(P<0.01)。结论金葡菌α溶血素诱导脐静脉内皮细胞凋亡的机制可能是通过TNF-α介导的caspase-8及caspase-3激活的外源性死亡因子受体途径,这为我们进一步研究金葡菌L型垂直感染与治疗提供了新的思路。
To study the apoptosis mechanism of human umbilical vein endothelial cells（HUVEC）induced by Staphylococcus aureus（S.aureus）α-hemolysin,HUVEC were infected by S.aureus α-hemolysin in different concentration for 8 hours.The quantity of TNF-α,caspase 3 and caspase 8 in supernatant were measured by colorimetric assay.After adding antibody against TNF-α and the inhibitor of caspase 3 or caspase 8,the apoptosis rates were detected by flow cytometry at the same time.The quantity of TNF-α,caspase 3 and caspase 8 were increased significantly in HUVEC infected with α-hemolysin compared to the control（P0.01）.However,the apoptosis rate of HUVEC was significantly inhibited by antibody against TNF-α and inhibitor of caspase 3 or caspase 8（P0.01）.It＇s suggested that the apoptosis mechanism of HUVEC induced by S.aureus α-hemolysin is probably by means of the exogenous death receptor activated by TNF-αmediated caspase 3 and caspase 8,which provide a new approach for further studies on vertical infection and treatment of S.aureus L-forms.
出处
《中国人兽共患病学报》
CAS
CSCD
北大核心
2010年第6期569-571,共3页
Chinese Journal of Zoonoses
基金
安徽省教育厅自然科学研究计划项目(No.2006KJ393B)
安徽省自然科学基金联合项目(No.01043706)
