单宁酸调控ATF6-CHOP通路增强顺铂诱导肝癌HepG2细胞凋亡的作用  

Tannic acid enhances cisplatin-induced apoptosis of hepatocellular carcinoma HepG2 cells by activating ATF6-CHOP pathway

作　　者：耿娜娜 吴明松 郑翔[3] 杨蕾[3] 王宏阳[3] 李学英 

机构地区：[1]贵州省普通高等学校口腔疾病研究特色重点实验室,医学与生物学研究中心,贵州遵义563000 [2]遵义医学院口腔学院,贵州遵义563000 [3]遵义医学院医学遗传学教研室,贵州遵义563000

出　　处：《实用医学杂志》2018年第1期12-15,共4页The Journal of Practical Medicine

基　　金：贵州省教育厅特色药用资源研发创新团队项目(编号：黔科合人才团队字[2013]15号); 贵州省科技厅资助项目(编号：黔科合LH字[2014]7548号); 遵义医学院硕士启动基金项目(编号：F-841);遵义医学院硕士启动基金项目(编号：F-827)

摘　　要：目的检测内质网应激ATF6-CHOP通路的激活水平,以探究单宁酸(TA)联合顺铂(CDDP)抗肝癌的分子机制。方法用180μmol/L TA、0.9μg/m L CDDP单独用药或者联合用药处理肝癌Hep G2细胞24和48 h后,利用实时荧光定量PCR(q-RT-PCR)、蛋白免疫印迹(Western Blot)技术检测细胞ATF6(ATF6α)、ATF6B(ATF6β)和CHOP的表达水平。结果药物处理24和48 h后,与对照组相比,TA组、CD-DP组和联合用药组ATF6 m RNA和蛋白水平、ATF6B蛋白水平、CHOP m RNA和蛋白水平均显著升高(P<0.01或P<0.05)。结论 TA能够联合CDDP增强肝癌Hep G2细胞内质网应激ATF6-CHOP通路的激活水平,ATF6-CHOP通路可能是TA和CDDP协同抗肝癌的分子机制之一。Objective To detect the activation levels of endoplasmic reticulum stress ATF6-CHOP path- way, and to investigate the molecular mechanism of tannic acid （TA） combined with cisplatin （CDDP） against he-patocellular carcinoma. Methods HepG2 cells were cultured with 180 μM TA or/and 0.9 μg/ml CDDP for 24 h or 48 h. The levels of ATF6 （ATF6α）, ATF6B （ATF6β） and CHOP were analyzed by real-time fluorescence quanti- tative PCR （q-RT-PCR） and western blot. Results We found that after 24 h or 48 h, compared with the control group, ATF6 mRNA and protein levels, ATF6B protein level, CHOP mRNA and protein levels were significantly increased in the TA group, CDDP group or combination group （P 〈 0.01 or P 〈 0.05）. Conclusion TA can com- bine with CDDP to increase the levels of endoplasmic reticulum stress ATF6-CHOP pathway, and the ATF6-CHOP pathway may be one of the molecular mechanisms synergistic anti-hepatocellular carcinoma effect of TA and CDDP on HenG2 cells.

关 键 词：单宁酸 顺铂 肝癌 内质网应激 转录活化因子6 C/EBP同源蛋白 

分 类 号：R735.7[医药卫生—肿瘤]