大黄素通过下调Prx V蛋白水平诱导AGS胃癌细胞凋亡  

AGS Gastric Cancer Cell Apoptosis Induced by Emodin through Down-regulate the Peroxiredoxin V Protein Level

作　　者：焦冰洋 王闯[1] 刘悦[1] 宫伊希 韩英浩[1] 金成浩[1] 崔玉东[1] 孙虎男[1] 

机构地区：[1]黑龙江八一农垦大学生命科学技术学院,大庆163319

出　　处：《黑龙江八一农垦大学学报》2018年第1期24-28,共5页journal of heilongjiang bayi agricultural university

基　　金：黑龙江八一农垦大学研究生创新科研项目(NO.YJSCX2016-Y44)

摘　　要：阐明大黄素(Emodin)诱导AGS人胃癌细胞凋亡过程中过氧化物还原酶5(Peroxiredoxin V;Prx V)的作用及其机制。为了检测大黄素对AGS人胃癌细胞的毒性作用,利用MTT法检测大黄素对AGS细胞存活率的影响。利用大黄素在不同浓度段(0,1,5,10,20,30μmol·L-1)和不同时间段(0,3,6,12,24 h)处理AGS细胞,用Annexin V-FITC和PE进行标记,利用流式细胞仪检测其凋亡情况,同时大黄素在不用时间段(0,3,6,12,24 h)处理AGS细胞,利用蛋白质免疫印迹法检测Prx V蛋白和凋亡相关蛋白的表达水平。结果显示,大黄素能够显著抑制AGS人胃癌细胞存活率,并呈时间和浓度依赖性地诱导细胞凋亡,同时伴随着活性氧(Reactive Oxygen Species,ROS)的升高,加入ROS清除剂NAC后,AGS细胞凋亡比率明显下降。大黄素通过显著抑制Prx V、Bcl-2和pro-caspase3蛋白质水平,上调Bad的表达诱导AGS细胞凋亡。研究表明,大黄素通过抑制Prx V蛋白水平,导致细胞内ROS水平升高,激活经典细胞凋亡途径导致AGS人胃癌细胞凋亡。To explore the regulatory effect of Prx V on AGS human gastric cancer cell apoptosis induced by emodin, cell viability was tested by MTI＇ assay,AGS cell apoptosis was detected by flow cytometry,the expression level of Prx V protein and apoptosis related protein was detected by western blotting. The results showed thatemodin could significantly inhibit the AGS human gastric cancer cell viability and cell apoptosis was induced in dose and time dependent manner,accompanied by up-regulating ROS. After adding ROS scavenger NAC,the apoptosis of AGS cell decreased significantly. Emodin through significantly down-regulated the Prx V, Bcl2, pro-caspase 3 protein levels and up-regulate bad protein level which respult in cell apoptosis. Our results showed that emodin exert anti-cancer properties by down-regulating the Prx V protein level which result in accumulated the cellular ROS levels. Subse- quently,it could activate the apopotic signalings increased the cell apoptosis in AGS gastric cancer cells.

关 键 词：大黄素 过氧化物还原酶5 活性氧 细胞凋亡 胃癌 

分 类 号：Q89[生物学]