GSH changes in HepG2 cells infected by dengue virus or stably expressing viral protein E and NS3

江雯; 田衍; 刘丽梅; 陈炜; 陈宗涛; 高娜; 徐小峰; 安静

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GSH changes in HepG2 cells infected by dengue virus or stably expressing viral protein E and NS3

更新时间：2026-01-09

- GSH changes in HepG2 cells infected by dengue virus or stably expressing viral protein E and NS3
- Journal of Army Medical University Vol. 29, Issue 24, Pages: 2311-2314(2007)
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  CLC： R373;R373.33;R394.2
- Published：2007
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江雯,田衍,刘丽梅,陈炜,陈宗涛,高娜,徐小峰,安静.登革病毒及其E蛋白和NS3蛋白对HepG2细胞中GSH水平的影响[J].陆军军医大学学报(原第三军医大学学报),2007,29(24):2311-2314.

　JIANG Wen,TIAN Yan-ping,LIU Li-mei,CHEN Wei,CHEN Zong-tao,GAO Na,XU Xiao-feng AN Jing.GSH changes in HepG2 cells infected by dengue virus or stably expressing viral protein E and NS3[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(24):2311-2314.
江雯,田衍,刘丽梅,陈炜,陈宗涛,高娜,徐小峰,安静.登革病毒及其E蛋白和NS3蛋白对HepG2细胞中GSH水平的影响[J].陆军军医大学学报(原第三军医大学学报),2007,29(24):2311-2314. DOI：

　JIANG Wen,TIAN Yan-ping,LIU Li-mei,CHEN Wei,CHEN Zong-tao,GAO Na,XU Xiao-feng AN Jing.GSH changes in HepG2 cells infected by dengue virus or stably expressing viral protein E and NS3[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(24):2311-2314. DOI：

摘要

目的通过对登革病毒感染后不同时相点以及稳定表达登革病毒E蛋白和NS3蛋白的HepG2细胞中GSH水平的测定，确定登革病毒感染后细胞内GSH水平的变化规律，以及登革病毒蛋白的表达对HepG2细胞内GSH水平的影响。方法用分光光度计比色定量检测登革病毒2型感染后不同时相点以及稳定表达登革病毒E蛋白和NS3蛋白的HepG2细胞中GSH水平的变化。结果总体来说，登革病毒2型感染后48 h内，HepG2细胞内GSH的水平呈下降趋势，其中以感染后的30 min、2 h和24 h细胞内GSH变化最为明显，与模拟感染组和其他时相点比较，均有显著差异；而稳定表达登革病毒E蛋白和NS3蛋白的HepG2细胞内GSH的水平也均较空质粒对照组降低。结论登革病毒2型感染HepG2细胞，可使细胞内的GSH下降，且呈现阶段性，推测可能与病毒的吸附、穿入、蛋白质合成、释放等过程有关，且登革病毒E蛋白和NS3蛋白在细胞内的表达也能一定程度地降低其GSH水平。

Abstract

Objective To investigate the changes of intracellular GSH content in HepG2 cells infected with dengue virus (DV) or stably expressing E or NS3 protein. Methods HepG2 cells were cocultured with DV or inactivitated DV

l h later the viral supernatant was removed. The infected HepG2 cells were collected 10

60 min

and 2

48 h after the beginning coculture and intracellular GSH content was detected by spectrophotometry. Intracellular GSH content was also detected in HepG2 cells stably expressing E protein/NS3 (pReceiver-E/HepG2

pReceiver-NS3/HepG2) and those containing empty plasmid (pReceiver/HepG2). Results GSH content showed a decreasing tendency after DV-2 infection. The lowest values were seen 30 min and 2

24 h after infection

which were of significant difference in comparison with those in inactivated DV infected HepG2 cells as well as at other time points. GSH levels in pReceiver-E/HepG2

pReceiverNS3/HepG2 were significantly lower than those in pReceiver/HepG2. Conclusion DV-2 infection might lead to the GSH depletion in HepG2 cells

and GSH lost from HepG2 cells might undergo a three-step process: virus adsorption/penetration

protein synthesis and budding. E or NS3 protein stably expressed in HepG2 cells can also decrease the GSH levels.

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