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目的 :探讨丁酸钠 (NaB)诱导人子宫内膜腺癌细胞 (HHUA)凋亡的机制。方法 :用终浓度 10mol L丁酸钠诱导HHUA细胞 ,以DNA荧光染色、琼脂糖凝胶电泳、流式细胞术 (FACS)等检测细胞凋亡的发生情况 ;用Westernblot分析细胞凋亡相关蛋白的表达以及caspase - 3及其抑制剂Ac -DEVD -CHO在NaB诱导细胞凋亡中的作用。结果 :NaB处理后 2 4hHHUA细胞即发生凋亡 ,Fas过度表达、caspase - 3激活及PARP被切割始于用药后 2 4h ,至 72h达高峰 ;Ac -DEVD -CHO能部分抑制NaB诱导的细胞凋亡。结论 :NaB诱导HHUA细胞凋亡与Fas过度表达和caspase - 3的激活有关。NaB可能成为一种新的抗子宫内膜癌药物
Objective: To investigate the mechanism of sodium butyrate (NaB) inducing apoptosis of human endometrial adenocarcinoma cells (HHUA). Methods: The HHUA cells were induced by sodium butyrate at the final concentration of 10 mol. The apoptosis of HHUA cells was detected by DNA fluorescence staining, agarose gel electrophoresis and flow cytometry (FACS). Western blot was used to analyze the expression of apoptosis related proteins And the role of caspase - 3 and its inhibitor Ac - DEVD - CHO in NaB - induced apoptosis. Results: Apoptosis occurred in HHUA cells 24 hours after NaB treatment. Fas - overexpression, activation of caspase - 3 and cleavage of PARP began at 24 hours and reached the peak at 72 hours after treatment. Ac - DEVD - CHO partially inhibited NaB - induced apoptosis Death. Conclusion: NaB - induced apoptosis in HHUA cells is related to overexpression of Fas and activation of caspase - 3. NaB may become a new anti-endometrial cancer drug