摘要
目的了解短链脂肪酸(SCFA)作用伤寒沙门菌诱导巨噬细胞凋亡机制。方法将SCFA作用伤寒沙门菌感染巨噬细胞8 h后,检测TNF-α、caspase3、caspase8、caspase9及NO的产生量,同时检测加入caspase3、caspase8、caspase9抑制剂和TNF-α抗体后的细胞凋亡率。结果作用8 h后caspase3、caspase8及NO、TNF-α的产生量均高于对照组(P<0.01)。caspase3、caspase8抑制剂和TNF-α抗体均能不同程度抑制SCFA作用伤寒沙门菌诱导的巨噬细胞凋亡(P<0.01)。结论 SCFA作用伤寒沙门菌诱导巨噬细胞凋亡可以通过NO及TNF-α介导,caspase3和caspase8参与的外源性凋亡途迳。
Objective To study the mechanism of macrophages apoptosis induced by short chain fatly acid（SCFA） stressed Salmonella typhi.Method The inhibitor of caspase3/8/9 and anti-TNF-α were added respectively in the macrophages before S.typhi.Apoptosis rates was determined by flow cytometry after infection for 8 h.The content of caspase3/8/9 and TNF-α and NO in macrophages after infected with SCFA stressed S.typhi on 8 h were detected.Result The apoptosis of macrophages were significantly inhibited by inhibitors of caspase3,caspase8 and antibody against TNF-α respectively（P〈0.01）.A significantly enhanced yield of caspase3 and caspase8 during macrophage apoptosis induced by SCFA stressed S.typhi correlated with the increased yield of TNF-α and NO（P〈0.01）.Conclusion The reactive TNF-α and NO induce caspase3 and caspase8 mediated apoptosis of macrophages by SCFA stressed S.typhi.
出处
《中国微生态学杂志》
CAS
CSCD
2010年第10期903-905,908,共4页
Chinese Journal of Microecology
基金
安徽省感染与免疫重点实验室课题(2004sys008)
蚌埠医学院科研项目(BY0808)
