摘要
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.
出处
《中华肿瘤防治杂志》
CAS
2006年第8期582-585,595,共5页
Chinese Journal of Cancer Prevention and Treatment