中华眼镜蛇毒诱导HL-60细胞凋亡及其机制探讨  

Possible mechanism of cobra venom serum of rabbit on apoptosis in HL-60 cells

作　　者：叶春玲[1] 张海伟[2] 罗英儒[1] 任先达[1] 郑佩娥[2] 刘建军[1] 李红良[1] 

机构地区：[1]暨南大学药学院药理学教研室,广州510632 [2]暨南大学医学院病理学教研室,广州510632

出　　处：《中国药理学通报》2003年第2期177-180,共4页Chinese Pharmacological Bulletin

基　　金：广东省科委博士启动基金资助课题 ;No 9740 2 6

摘　　要：目的　观察中华眼镜蛇毒体外对白血病细胞凋亡的影响 ,并探讨其可能的作用机制。方法　本研究采用血清药理学方法 ,以人白血病细胞HL 60细胞为靶细胞 ,通过流式细胞仪分析、DNA片段凝胶电泳、免疫组织化学 (S P法 )观察中华眼镜蛇毒兔血清体外对细胞凋亡的诱导作用及癌基因表达的影响。结果　经DNA电泳、流式细胞仪分析显示 :中华眼镜蛇毒兔血清与HL 60细胞共同培养 48h可诱导其细胞凋亡增加 ,bcl 2、c myc基因蛋白表达下调。结论　中华眼镜蛇毒兔血清体外抑制HL 60细胞增殖可能与其诱导细胞凋亡及使细胞bcl 2、cAIM To explore the effect of CVSR on the apoptosis in leukemia cells and its possible mechanism. METHODS Serologic test was adopted and by means of the agarose gel electrophoresis together with flow cytometry analyse, the HL-60 cells were used as a target to study the apoptosis after the action of CVSR. RESULTS A characteristic DNA 'ladder' was detected by using agarose gel electrophoresis. By flow cytometry analysis, it was found that most apoptosis of HL-60 cells occurred when cultured with CVSR for 48 hours. Through immunohistochemistry, it was suggested that bcl-2 and c-myc gene protein expression of HL-60 cells was down-regulated. CONCLUSION CVSR inhibited the HL-60 cells in vitro which was probably related to cell apoptosis and down-regulation of bcl-2, c-myc gene protein expression.

关 键 词：中华眼镜蛇毒 白血病 细胞凋亡 HL-60细胞 

分 类 号：R282.74[医药卫生—中药学]