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目的探讨非甾体药物选择性环氧合酶-2(COX-2)抑制剂NS398对白血病细胞株K562细胞增殖及凋亡的效应关系和机制。方法采用噻唑蓝还原法(MTT法)检测NS398对K562细胞增殖抑制作用,流式细胞仪(FCM)和单细胞凝胶电泳技术(cometassay)测定K562细胞的凋亡,免疫印迹实验检测相关蛋白的表达。结果 NS398抑制K562细胞增殖存在时间和剂量效应关系,各浓度间差异有显著性(P<0.05)。NS398激活caspase-3和caspase-9,促进P53蛋白的积聚、Bax蛋白表达的上调和Bcl-xL蛋白表达的下调,进而导致细胞色素C的释放,致使K562细胞凋亡。结论 NS398可抑制K562细胞增殖,其诱导细胞凋亡的途径可能经过P53介导Bax的Caspase-3、Caspase-9的激活,揭示COX-2抑制剂可能存在着一个影响细胞翻译的新机制。
Objective To investigate the effect and mechanism of NS398, a non-steroidal drug-selective cyclooxygenase-2 (COX-2) inhibitor, on the proliferation and apoptosis of leukemia cell line K562. Methods The inhibitory effect of NS398 on the proliferation of K562 cells was detected by MTT method. The apoptosis of K562 cells was determined by flow cytometry (FCM) and single cell gel electrophoresis (cometassay). The expression of related proteins expression. Results The NS398 inhibited the proliferation of K562 cells in a time and dose-dependent manner. There was a significant difference between the concentrations of NS398 (P <0.05). NS398 activates caspase-3 and caspase-9 to promote the accumulation of P53 protein, the up-regulation of Bax protein expression and the down-regulation of Bcl-xL protein expression, leading to the release of cytochrome C and the apoptosis of K562 cells. Conclusion NS398 can inhibit the proliferation of K562 cells. The pathway of apoptosis induced by NS398 may be mediated by P53 and Caspase-3, Caspase-9 activation of Bax, suggesting that COX-2 inhibitors may have a new mechanism of affecting cell translation.