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戊地昔布对人结肠癌HT-29细胞凋亡的影响

Effects of Valdecoxib on HT-29 cells Apoptosis

  • 摘要: 目的 观察戊地昔布(Valdecoxib)对COX-2高表达的人结肠癌HT-29细胞凋亡的影响。方法 将体外培养HT-29细胞分为正常组(C)、药物处理组(V)及溶剂对照组(S)。采用流式细胞术检测细胞凋亡,Western blot检测COX-2、caspase-3、cleaved caspase-3、Bcl-2、p38 MAPK、p-p38 MAPK。结果 与正常组相比,药物处理组细胞凋亡明显增加(P<0.05),cleaved caspase-3和p-p38 MAPK表达增高,Bax/Bcl-2比率明显升高(P<0.05)。Valdecoxib干预能够显著促进HT-29细胞凋亡,上调cleaved caspase-3和p-p38 MAPK的表达,增加Bax/Bcl-2比率。 结论 COX-2选择性抑制剂Valdecoxib 能够促进HT-29细胞凋亡部分可能是通过激活p38MAPK信号通路而实现的。

     

    Abstract: Objective To investigate the effects of a non-steroidal anti-infl ammatory drug(Valdecoxib)on human colon cancer HT-29 cell lines. Methods In vitro cultured HT-29 were divided into normal group(C), Valdecoxib group(V) and solvent control group(S). Apoptosis of HT-29 was analyzed by fl ow cytometry. The expression levels of COX-2, caspase-3, cleaved caspase-3, Bax, Bcl-2, p38 MAPK and p-p38 MAPK protein were detected by Western blot. Results Compared with normal group(C), cell apoptosis, the expression of cleaved caspase-3 and p-p38 MAPK and the ratio of Bax/Bcl-2 were signifi cantly increased in Valdecoxib group(V) (P<0.05). Valdecoxib interference could significantly promote cell apoptosis, the expression of cleaved caspase-3 and p-p38 MAPK, and the ratio of Bax/Bcl-2 in HT-29. Conclusion The inhibition effects of Valdecoxib on HT-29 apoptosis may be related with activating p38MAPK signal pathway.

     

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