内吗啡肽-1诱导K562细胞凋亡的实验研究

Experimental study on EM-1 inducing K562 cell apoptosis

目的:探讨内吗啡肽1(endomorph ine1,EM1)诱导人类慢性髓性白血病K562细胞株的凋亡作用。方法:采用MTT法检测EM1对K562细胞的增殖抑制作用;瑞士吉姆萨染色和荧光显微镜观察细胞形态变化;流式细胞术(FCM)和琼脂糖凝胶电泳测定细胞凋亡,免疫组化探讨其机制。结果:EM1能明显抑制K562细胞增殖,使K562细胞出现凋亡所具有的形态学及生物化学特征,同时对K562细胞的增殖抑制和诱导凋亡作用具有时间依赖性和剂量依赖性。与对照组相比,细胞抑制率和凋亡率差异有统计学意义,P<0.01。bcl2表达降低,bax表达增高。结论:EM1能诱导K562细胞凋亡,抑制肿瘤细胞增殖呈一定的浓度和时间依赖关系,其作用机制可能与bcl2/bax通路激活有关。

OBJECTIVE ： To investigate the effection of endomorphine-1 （EM-1） on K562 in vitro. METHODS： Inhibition of K562 cells proliferation was measured by MTT assay. Morphological assessment of apoptosis was performed with Wright-Gimsa staining and fluorescence microscopey. The apoptosis peak was measured by flow cytometry. DNA fragmenatation was visualized by agarose gel electrophoresis. The mechanism of apoptosis was studied by immunohistochemistry. RESULTS： EM-1 time-dependently and dose-dependently inhibited the proliferation of K562 cells, which displayed the apoptosis characteristics of morphology and biochemistry. Compared with the contrast, there was a significant difference in cell inhibition and apoptosis ratio （P〈0.01）. The expression of bcl-2 was decreased, but the expression of bax increased. CONCLUSION： EM-1 could induce K562 cells apoptosis time-dependently and dose-dependently, The mechanism of action could be related to bcl-2/bax access activated.