Piscidinol A诱导人白血病K562细胞凋亡及其作用机制

Piscidinol A Induce Leukemia K562 Cells Apoptosis and Its Preliminary Mechanism

目的:初步研究Piscidinol A对人慢性髓系白血病K562细胞的增殖抑制作用及抗肿瘤分子作用机制。方法:MTT法检测细胞增殖抑制率;Hoechst 33258染色法检测细胞凋亡形态;AnnexinⅤ-FITC/PI双标记法检测细胞凋亡率;Western blot方法检测Piscidinol A对细胞中凋亡相关蛋白表达的影响。结果:Piscidinol A对K562细胞具有增殖抑制作用且呈浓度和时间依赖关系,24 h时IC_(50)为27.36 mg/L;细胞凋亡染色示有典型的细胞凋亡形态出现;流式细胞仪AnnexinⅤ-FITC/PI双标记法检测发现Piscidinol A可诱导K562细胞凋亡,其凋亡率呈浓度依赖性;Western blot法检测到Piscidinol A能上调Bax和Caspase-3的表达,同时下调抑凋亡蛋白Bcl-2的表达。结论:Piscidinol A能抑制K562细胞增殖并诱导其凋亡,其作用机制可能与凋亡相关蛋白表达量变化有关。

Objective：To elucidate the anticancer effects and its mechanism of Piscidinol A induced on the leukemia K562 cell line. Methods：MTT assay was applied to determine cell survival rate. The morphology of apoptotic cells was observed by Hoechst 33258 fluorescence staining. The apoptosis rate of K562 cell was detected by AnnexinV-FITC/PI double staining. Western blot was applied to detect apoptosis related proteins expression. Results：Piscidinol A had remarkable proliferation inhibition effect on K562 cell in a dose and time-dependent manner ,the IC50 was 27. 36 mg/L at 24 h. Most of cells presented the typical morphological changes of apoptosis by fluorescent microscope. The apoptosis of K562 cell line could be induced by Piscidinol A and the level increased following with the aug- mentation of Piscidinol A concentration increasing. Western blot disclosed that Piscidinol A could up-regulate the expression of Caspase- 3 and Bax,while down-regulate anti-apoptotic Bcl-2 protein expression. Conelusion：Piscidino｜ A has the inhibition effect on the prolifer- ation and can induce apoptosis of K562 cell line in vitro, and the mechanism may be related to the change of apoptosis related protein expression.