尼莫地平对阿糖胞苷诱导HL-60细胞凋亡机制影响的研究  

Effect of Nimodipine on Mechanisms of HL-60 Cell Apoptosis Induced by Cytarabine

作　　者：孙立荣[1] 高彬昌[1] 庞秀英[1] 卢愿[1] 李学荣[1] 宋爱琴[1] 

机构地区：[1]青岛大学医学院附属医院儿科,青岛266003

出　　处：《中国实验血液学杂志》2007年第1期72-75,共4页Journal of Experimental Hematology

摘　　要：为了研究尼莫地平对阿糖胞苷诱导HL-60细胞凋亡机制的影响,采用琼脂糖凝胶电泳检测其DNA凋亡带,用细胞免疫组织化学方法检测细胞凋亡相关基因bcl-2、bax的蛋白表达。结果表明,实验组自培养8小时起琼脂糖凝胶电泳显示典型的DNA梯形凋亡带。Bcl-2蛋白表达在各实验组随培养时间延长逐渐下降,而Bax蛋白的表达则逐渐增加,Bcl-2/Bax比值逐渐下降,8小时就与对照组出现差异(P<0.05)。结论:尼莫地平及阿糖胞苷均能促进HL-60细胞凋亡,诱导其凋亡的机制与下调bcl-2及上调bax基因的蛋白表达有关。尼莫地平能加强阿糖胞苷促进HL-60细胞凋亡,其机制与协同下调bcl-2的表达有关。The aim was to study the mechanisms of HL-60 cell apoptosis induced by nimodipine （ NMDP ） and cytarabine （Ara-C）. The DNA fragment was detected by agarose gel electrophoresis. The expressions of bcl-2 and bax gene proteins related with apoptosis were investigated by immunohistochernistry. The results showed that HL-60 cell apoptosis rate had been increasing in the experimental groups compared with the control group since culturing 8 hours. The expression of Bcl-2 protein was lower and the expression of Bax protein was higher in the experimental groups than that in the control group, while ratio of bcl-2/bax was lower in the experimental groups than that in the control group. It is concluded that NMDP and Ara-C induce apoptosis of HL-60 cells, and the mechanism of apoptosis induced by them may down-regulate the expression of bcl-2 gene and up-regulate the expression of bax gene. The mechanism of HL-60 cell apoptosis induced by Ara-C and NMDP is probably associated with the down-regulation of Bcl-2 protein expression.

关 键 词：尼莫地平 阿糖胞苷 凋亡 HL-60细胞系 蛋白表达 Bcl-2 Bax 

分 类 号：R733.7[医药卫生—肿瘤] R979.1[医药卫生—临床医学]