抑制ERK1/2通路对卡铂诱导人卵巢癌细胞凋亡的影响  

Effects of carboplatin inducing apoptosis in human ovarian cancer cells through inhibiting ERK1/2 pathway

作　　者：李兴媚[1] 郑立红[2] 刘丹[2] 李跃文[1] 梅庆步[2] 董冰[1] 

机构地区：[1]齐齐哈尔医学院附属第三医院妇产科,齐齐哈尔161001 [2]齐齐哈尔医学院基础医学院生物遗传教研室

出　　处：《陕西医学杂志》2016年第5期522-524,538,共4页Shaanxi Medical Journal

基　　金：黑龙江省卫生计生委科学技术研究项目(2013173)

摘　　要：目的:探讨抑制ERK1/2通路对卡铂诱导卵巢癌细胞凋亡作用的影响。方法:采用Hoechst 33258荧光染色法检测抑制ERK1/2通路对卡铂诱导卵巢癌HO-8910细胞凋亡的影响;用分光光度法检测卡铂浓度的增加及抑制ERK1/2通路对卵巢癌HO-8910细胞Caspase-8和Caspase-9活化的影响。结果:CBP组、PD98059组及联用组部分细胞核呈现亮蓝色荧光的为凋亡细胞,细胞核可见碎块状荧光信号,凋亡指数CBP组为20.35%,PD98059组为15.21%,联用组为29.78%。随着卡铂浓度的增加,Caspase-8、Caspase-9活性的改变并不明显(P>0.05),而联用组的Caspase-8、Caspase-9活性最高,抑制ERK1/2通路可促进卡铂增强Caspase-8、Caspase-9的活性(P<0.01)。结论:抑制ERK1/2通路可促进卡铂诱导卵巢癌细胞凋亡作用,并与Caspase-8、Caspase-9活化有关。Objective：To explore the impacts of cell apoptosis treated by carboplatin in ovarian cancer cells through inhibiting ERK1/2pathway.Methods：Hoechst 33258 assay was used to detect the effects of carboplatin inducing apoptosis in human ovarian cancer HO-8910 Cells through inhibiting ERK1/2pathway.Spectrophotometry was used to detect the impacts of activation of Caspase-8and Caspase-9through increasing the concentration of carboplatin and inhibiting ERK1/2pathway.Results：The nucleus of all drug groups appeared bright blue fluorescence,they were apoptotic cells.Some nuclei had fragmental fluorescence.Apoptosis index,CBP group was 20.35%,PD98059 group was 15.21%,combined group was 29.78%.The activities of Caspase-8and Caspase-9changed were not obvious,with increasing concentrations of carboplatin（P〉0.05）.And combined group＇s activities were the highest.Inhibition of ERK1/2pathway could help carboplatin increasing Caspase-8and Caspase-9（P〈0.01）.Conclusion：Inhibition of ERK1/2pathway can promote carboplatin inducing cell apoptosis in human ovarian cancer cells,and it relates to caspase-8and caspase-9activations.

关 键 词：卵巢肿瘤/化学诱导 卵巢肿瘤/预防和控制 卡铂/治疗应用 有丝分裂素激活蛋白激酶类/代谢 半胱氨酸内肽酶类/代谢 

分 类 号：R737.31[医药卫生—肿瘤]