摘要
目的:观察黄芪联合恩替卡韦对转染了乙肝病毒(HBV)的Hep G2.2.15细胞JAK-STAT通路mRNA的影响,探讨两者可能存在的抗HBV的作用机理。方法:将未转染乙肝病毒的Hep G2细胞设为空白对照组,而转染了乙肝病毒的Hep G2.2.15细胞分为恩替卡韦治疗组,黄芪高、中、低剂量治疗组,黄芪高、中、低剂量联合恩替卡韦治疗组及模型对照组,每组3个复孔。检测各组JAK-STAT通路中转录活化因子1、2(STAT1、STAT2)、干扰素刺激基因因子3(ISGF3)、2'5'寡腺苷酸合成酶(2'5'OAS)、RNA依赖蛋白激酶(PKR)的mRNA表达水平,并进行统计学分析。结果:与空白组比较,病毒对照组JAK-STAT通路的ISGF3 mRNA表达下降明显(P<0.05)。较之病毒对照组,恩替卡韦组和中低剂量的联合用药组可使表达下降的ISGF3mRNA表达增强(P<0.05),而联合用药组ISGF3mRNA的表达水平和空白对照组相当(P>0.05)。与空白对照组相比,病毒对照组STAT2mRNA的表达没有差异(P>0.05),恩替卡韦组可上调正常表达的STAT2 mRNA(P<0.05),黄芪组STAT2mRNA的表达虽然和病毒对照组没有差异(P>0.05),但是其高、中剂量组和空白对照组却表现出来了差异(P<0.05或0.01)。与病毒对照组相比,各组STAT1、2'5'OAS、PKR的mRNA表达没有变化(P>0.05)。结论:黄芪注射液联合恩替卡韦抗HBV的机理可能和受病毒感染肝细胞JAK-STAT信号通路ISGF3蛋白的表达恢复有关。同时两药物对该通路中STAT2蛋白活性调节可能存在的互补作用说明两药物联合使用在预防肝细胞癌方面具有一定的意义。
Objective ： To observe Huangqi （ HQ） and Entecavir on the mRNA of JAK - STAT pathway in HepG2. 2 .15 cell infected with Hepatitis B virus （HBY） , and to explore its mechanism. Methods： HepG2 cells were put into blank control group,HepG2.2 .1 5 cells were divided into entecavir group, HQ high, medium and low dose groups, HQ high, medium and low - dose combinated with Ente-cavir groups and model control group with 3 wells each group. The JAK - STAT pathway transcriptional activator 1,2 （ STAT1, STAT2） , interferon stimulated gene factor3 （ISGF3） ,25bligoadenylate synthetase （250AS） , RNA dependent protein kinase （PKR） mRNA expression levels were detected and statistical analysised. Results ： Compared with the blank control group, in virus control group JAK - STAT pathway ISGF3 mRNA expression was significantly decreased（P 〈0.05）. Yet,compared with the virus control group, IS- GF - 3 mRNA expression increased in the Entecavir group and the medium and low - doses HQ combined with Enticavir groups （ P 〈0.05）. Yet,ISGF3 mRNA of the drugs combination groups was equal to the blank control group. Compared with the blank controlgroup,STAT2 mRNA expressions of the virus control group have no difference with it（P 〉0. 05） ,but the normal expression of it wasbroken and rose in the Enticavir group. （P 〈0. 05）. While the expression of STAT2mRNA have no difference with the virus controlgroup,High and medium dose groups have differences（P 〉0. 05 or 0. 01） Conlusion：The mechanism HBVDNA quantitation reboundslowly of HQ combined with Entecavir for discontinuation of drugs may be related to ISGF3 protein expression recovery of JAK - STATsignaling pathways. At the same time,the different effect of two drugs on regulating of STAT2 mRNA of this singaling pathway showedthere are some differences and complementaries on STAT2 protein activities resulted from their pesticide effect. The effects of STAT2protein may closely related to drugsdrug conce
出处
《江西中医药大学学报》
2017年第3期82-86,共5页
Journal of Jiangxi University of Chinese Medicine
基金
广州市科技和信息化局项目(201300000142)
