雷公藤内酯醇通过调控miR-194的表达诱导肝癌HepG2细胞凋亡和自噬  

Triptolide induces apoptosis and autophagy in HepG2 cells by regulating the expression of mir-194

作　　者：李春雨 杨航[2] LI Chun-yu;YANG Hang(Shenzhen Longhua District Central Hospital Longhua Central Hospital Affiliated to Guangdong Medical University,Shenzhen 518110,China;Department of oncology,Wuhan integrated traditional Chinese and western medicine hospital,Wuhan 430000,China)

机构地区：[1]深圳市龙华区中心医院广东医科大学附属龙华中心医院,广东深圳518110 [2]武汉市中西医结合医院肿瘤科,湖北武汉430000

出　　处：《吉林医学》2022年第1期7-11,共5页Jilin Medical Journal

摘　　要：目的:研究雷公藤内酯醇通过调节微小RNA-194(miR-194)表达对肝癌HepG2细胞活力、凋亡和自噬的影响。方法:将HepG2细胞分为对照组及10 nmol/L、20 nmol/L、40 nmol/L、60 nmol/L和80 nmol/L雷公藤内酯醇处理组,采用MTT法和Western印迹实验检测各组HepG2细胞的活力、凋亡及自噬蛋白表达;RT-qPCR检测各组HepG2细胞中miR-194的表达。转染miR-194模拟物(miR-194 mimic)及阴性对照(miR-194 NC)至HepG2细胞,检测miR-194 mimic和miR-194 NC在雷公藤内酯醇处理后对HepG2细胞活力的影响,Western印迹检测凋亡和自噬标志蛋白LC3-Ⅰ、LC3-Ⅱ、Beclin-1、Bax、Bcl-2和Caspase-3的蛋白表达。结果:与对照组相比,不同浓度的雷公藤内酯醇可抑制HepG2细胞的活力并促进其凋亡和自噬,差异有统计学意义(P<0.05)。雷公藤内酯醇可上调HepG2细胞中miR-194的表达,并具有剂量依赖性,差异有统计学意义(P<0.05),同时促使Bax/Bcl-2的比值和Caspase-3蛋白的表达升高,差异有统计学意义(P<0.05),使LC3和Beclin-1蛋白表达量升高,差异有统计学意义(P<0.05)。miR-194 mimic可增加雷公藤内酯醇对HepG2细胞活力的抑制,并进一步促进凋亡和自噬。结论:雷公藤内酯醇可能通过上调miR-194表达抑制肝癌HepG2细胞生长并促进其凋亡和自噬。Objective To analyze the effect of triptolide on the proliferation,apoptosis and autophagy of HepG2 cells by modulating the expression of miR-194.Method HepG2 cells were divided into control group,10 nmol/L,20 nmol/L,40 nmol/L,60 nmol/L and 80 nmol/L TPL group,MTT assay and Western blot were used to detect the cells activities and proteins expression relevant to apoptosis and autophagy;RT-qPCR was used to evaluate the expression of miR-194 of HepG2 cells.Transfecting miR-194 mimic and miR-194 NC to HepG2 cells,detecting the influences of miR-194 mimic and miR-194 NC on the viability of Hep2 cells after treated with TPL.The expressions of LC3-Ⅰ,LC3-Ⅱ,Beclin-1,Bax,Bcl-2 and Caspase-3 were detected by western blot.Results Compared with control group,TPL treated groups inhibited the activities of HepG2 cells and promoted its apoptosis and autophagy(P<0.05).TPL up-regulated the miR-194 expression of HepG2 cells with dose-dependent(P<0.05)and up-regulated the ratio of Bax/Bcl-2 and Caspase-3 expression(P<0.05),up-regulated the LC3 and Beclin-1 expression(P<0.05).miR-194 mimic enhanced the suppression of TPL on the inhibition of HepG2 cells and promoted its apoptosis and autophagy.Conclusion TPL could promote HepG2 cells apoptosis and autophagy by up-regulating miR-194 expression.

关 键 词：雷公藤内酯 肝癌 miR-194 凋亡 自噬 

分 类 号：R285[医药卫生—中药学]