【摘要】 目的研究5-氟尿嘧啶(5-Fu)诱导人结肠癌细胞(HCT116)凋亡与核转录因子-κB(NF-κB)活化以及尿激酶型纤溶酶原激活物(uPA)表达的关系,并观察吡咯烷二硫氨基甲酸盐(PDTC)抑制 NF-κB活化对5-Fu 诱导结肠癌细胞凋亡及 uPA 表达的影响。方法采用流式细胞仪Annexin V-FITC 法检测结肠癌细胞 HCT116凋亡;采用免疫组织化学方法半定量分析 HCT116细胞NF-κB及 uPA 表达的动态变化。结果 5-Fu 在诱导 HCT116细胞凋亡的同时有 NF-κB活化,1μmol/L PDTC 能显著增加5-Fu 诱导 HCT116细胞凋亡及抑制5-Fu 诱导的 HCT116细胞 NF-κB活化作用(P<0.05),uPA 变化与 NF-κB一致。结论 5-Fu 在诱导 HCT116细胞凋亡的同时活化了NF-κB,uPA 表达亦随之增强;PDTC 在抑制5-Fu 诱导的 HCT116细胞 NF-κB活化的同时增强了5-Fu 诱导细胞凋亡的作用,uPA 表达也相应下降。更多还原

【Abstract】 Objective To study the relationship among apoptosis,NF-KB activation and uPA expres- sion in human colon carcinoma cell line HCTll6 induced by 5-fluorouracil,and to observe the effect of in- hibiting activity of NF-KB by PDTC on apoptosis as well as expression of uPA.Methods Cell apoptosis was analysed by Annexin V-FITC.Fluctuation of NF-KB and uPA was detected by semi-quantitative immuno- histochemistry.Results 5-fluorouracil could induce apoptosis and activate NF-KB.PDTC could significantly increase the apoptosis and suppress the activation of NF-KB induced by 5-fluorouracil.There was a positive correlation between the changes of uPA and NF-KB.Conclusion 5-fluorouracil could induce apoptosis,ac- tivate NF-KB and up-regulate expression of uPA of HCT116 cells.The mechanism of enhanced apoptosis by PDTC may be related to suppressing activation of NF-κB and down-regulating expression of uPA.更多还原