硼酸钠活化p53诱导人肝癌细胞HepG2凋亡  

Apoptosis of human hepatocellular carcinoma cell HepG2 induced by borax-activated p53

作　　者：魏英[1] 张有顺[2] 武伦 袁方均[2] 陈琴华[1] 周文波[2] 

机构地区：[1]湖北医药学院附属东风医院实验中心,湖北十堰442000 [2]湖北医药学院附属东风医院肝胆外科,湖北十堰442000

出　　处：《实用药物与临床》2016年第12期1478-1482,共5页Practical Pharmacy and Clinical Remedies

基　　金：十堰市科技局基金(15Y56);湖北省自然科学基金面上基金(2015CFB615)

摘　　要：目的观察硼酸钠(Borax)对人肝癌细胞株Hep G2的生长抑制和诱导凋亡的作用,并初步探讨其作用机制。方法采用MTT法检测不同浓度硼酸钠对Hep G2活力的影响,DAPI染色荧光显微镜及Annexin V-FITC/PI双染色流式细胞术检测硼酸钠诱导细胞凋亡的情况。实时荧光定量PCR(qRT-PCR)检测硼酸钠对肿瘤抑制因子p53及其下游基因Bcl-2、Bax、Noxa、Puma mRNA表达的影响。结果与对照组比较,硼酸钠各剂量组均能抑制Hep G2的活力(P<0.01);硼酸钠诱导Hep G2细胞凋亡,不同浓度硼酸钠(0、1.0、2.0、4.0 mmol/L)处理24 h后,晚期凋亡细胞百分比从2.57%分别增加至8.13%、10.4%、15.24%,差异有统计学意义(P<0.01);硼酸钠(4.0 mmol/L)分别作用6、12、24 h后,均可不同程度上调肿瘤抑制因子p53及促凋亡基因Bax、Noxa、Puma mRNA表达,抑制抗凋亡基因Bcl-2 mRNA的表达,差异有统计学意义(P<0.01)。结论硼酸钠抑制人肝癌细胞Hep G2的生长活性并诱导凋亡,其机制与p53的活化及其下游Bax、Noxa、Puma基因表达上调,以及Bcl-2表达下调有关。Objective To observe the effect of borax on the growth inhibition and apoptosis of human hepatocellular carcinoma cell line HepG2,and to explore its mechanism.Methods The potential effect of borax on the cell viability was examined using MTT assay.The cell apoptosis rate of cells treated with borax was analyzed by DAPI and Annexin V-FITC/PI staining.The level of tumor suppressor factor p53 and its downstream gene Bcl-2,Bax,Noxa Puma mRNA were detected by real-time PCR.Results Compared with control group,borax in different dose group could inhibit the activity of HepG2（P〈0.01）.Borax induced apoptosis of HepG2 cells,and after 0,1.0,2.0,4.0 mmol/L borax treat 24 h,the percentage of late apoptotic cell increased from 2.57%to 8.13%,10.4%and 15.24%respectively（P〈0.01）,the difference being of statistical significance.After 4.0 mmol/L borax treatment for 6,12,24 h,the tumor inhibition factor p53 and pro-apoptotic gene Bax,noxa,puma mRNA expression significantly increased,but the anti-apoptosis gene Bcl-2 mRNA expression was significantly down-regulated（P〈0.01）.Conclusion Borax inhibits the growth of human hepato cellular carcinoma cell HepG2 activity and induces apoptosis.The mechanism may be related to the activation of p53,up-regulation of Bax,Noxa and Puma mRNA expression,and down-regulation of Bcl-2 mRNA expression.

关 键 词：硼酸钠 人肝癌细胞株HEPG2 凋亡 P53 BCL-2 

分 类 号：R735.7[医药卫生—肿瘤]