HuH7.5.1细胞中利巴韦林对聚乙二醇干扰素诱导的抗病毒蛋白PKR的影响及机制研究  

Effect and Mechanism of Ribavirin on Peg-IFN-inducible Antiviral Protein PKR in Huh7.5.1 Cells

作　　者：潘颖 杨凯 王传博[2] PAN Ying;YANG Kai;WANG Chuanbo(Anhui Medical College;The Second Affiliated Hospital Of Anhui Medical,Anhui,Hefei 230601,China)

机构地区：[1]安徽医学高等专科学校 [2]安徽医科大学第二附属医院,安徽合肥230601

出　　处：《九江学院学报（自然科学版）》2021年第3期81-84,共4页Journal of Jiujiang University：Natural Science Edition

基　　金：国家自然科学基金(编号81202808);安徽高校自然科学研究项目(编号KJ2020A0861);安医专校级一般科研项目(编号YZ2020ZR007)的成果之一。

摘　　要：目的探讨在HuH7.5.1细胞中,利巴韦林对聚乙二醇干扰素诱导的抗病毒蛋白PKR的影响及其机制。方法将HuH7.5.1细胞分为4组:对照组、干扰素组、利巴韦林组和联合组,对照组细胞给予PBS处理,干扰素组细胞给予400IU/mL干扰素处理,利巴韦林组细胞给予80μg/mL利巴韦林处理,联合组细胞给予400IU/mL干扰素联合80μg/mL利巴韦林处理。运用免疫印迹(Western-blot)技术分析各组细胞内p-PKR、PKR、STAT1、p-STAT1等蛋白的表达。结果与对照组细胞相比,干扰素组、利巴韦林组及联合组细胞内p-PKR蛋白、PKR蛋白、p-STAT1蛋白及STAT1蛋白水平均显著升高,差异具有统计学意义(p<0.05),且与干扰素组相比,联合组细胞内的变化趋势更为明显(p<0.05)。而p-ERK1/2蛋白含量在干扰素组、利巴韦林组及联合组细胞中均低于对照组细胞(p<0.05),且在联合组细胞内明显低于干扰素组及对照组细胞,差异具有统计学意义(p<0.05)。结论利巴韦林可能通过抑制ERK蛋白的活化,从而上调干扰素诱导的JAK-STAT信号转导通路,增强抗病毒蛋白PKR的表达。Objective To investigate the effect of Ribavirin(RBV)on the antiviral protein PKR induced by Peg-IFN in HuH7.5.1 cells and to explore its relevant mechanism.Method HuH7.5.1 cells were divided into four groups:control group,IFN group,RBV group and combined group.The control group cells were treated with PBS,the IFN group cells were treated with 400 IU/ml of Peg-IFN,the RBV group cells were treated with 80μg/ml ribavirin,and the combined group cells were treated with 400 IU/ml of Peg-IFN plus 80μg/ml ribavirin.Western blot was used to determine the relative expression of p-PKR、PKR、STAT1、p-STAT1 proteins in cells of each group.Result Compared with the control group,the relative expressions of p-PKR、PKR、STAT1、p-STAT1 proteins in cells of IFN group,RBV group and combined group,were significantly higher(p<0.05),and the levels of these proteins in combined group cells were significantly higher than those in the IFN group cells(p<0.05).However,the levels of p-ERK in the cells of IFN group,RBV group and combined group were all further decreased,compared with the control group(p<0.05),similarly,the relative expression of p-ERK in the combined group cells was significantly lower than that in the IFN group cells(p<0.05).Conclusion Ribavirin could induce the synthesis of the antiviral protein PKR by upregulating the IFN-induced JAK-STAT signal transduction pathway,and it was possibley achieved this by inhibiting ERK activation in Huh7.5.1 cells.

关 键 词：聚乙二醇干扰素 利巴韦林 PKR蛋白 STAT1蛋白 

分 类 号：R587.1[医药卫生—内分泌]