短链脂肪酸作用下伤寒沙门菌诱导巨噬细胞凋亡机制的探讨

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(P0.01)。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(P0.01)。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。

Mechanism of macrophages apoptosis induced by short chain fatly acid stressed Salmonella typhi

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.