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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 understand the mechanism of short chain fatty acid (SCFA) -induced Salmonella typhimurium-induced macrophage apoptosis. Methods The levels of TNF-α, caspase3, caspase8, caspase9 and NO were detected after SCFA treatment of typhimurium-infected macrophages for 8 h. At the same time, the apoptosis of cells was detected by addition of caspase3, caspase8, caspase9 and TNF- Death rate. Results After 8 h, the production of caspase 3, caspase 8, NO and TNF-α were higher than those of the control group (P <0.01). Both caspase3, caspase8 inhibitor and TNF-α antibody could inhibit SCFA-induced Salmonella typhimurium-induced apoptosis of macrophages to varying degrees (P <0.01). Conclusion SCFA induced the apoptosis of macrophages by Salmonella typhimurium mediated by NO and TNF-α, caspase3 and caspase8 involved in extrinsic apoptotic pathway.