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谷胱甘肽对登革病毒产生的抑制作用。

Inhibitory effects of glutathione on dengue virus production.

作者信息

Tian Yanping, Jiang Wen, Gao Na, Zhang Junlei, Chen Wei, Fan Dongying, Zhou Deshan, An Jing

机构信息

Department of Histology and Embryology, School of Basic Medicine, Third Military Medical University, Chongqing 400038, PR China.

出版信息

Biochem Biophys Res Commun. 2010 Jul 2;397(3):420-4. doi: 10.1016/j.bbrc.2010.05.108. Epub 2010 May 27.

DOI:10.1016/j.bbrc.2010.05.108
PMID:20510876
Abstract

Reduced glutathione (GSH) is the most powerful intracellular antioxidant and also involved in viral infections. The pathogenesis of dengue virus (DV) infection has not been completely clarified. This study investigated the relationship between DV serotype 2 (DV2) infections and host intracellular GSH content. Results showed infection with DV2 resulted in a decrease in intracellular GSH, which caused NF-kappaB activation and increased DV2 production. Supplemental GSH significantly inhibited activation of NF-kappaB, resulting in a decreased production of DV2 in HepG2 cells. Furthermore, high activity of NF-kappaB and increased production of DV2 was observed in HepG2 cells treated with buthionine sulfoximine (BSO), an inhibitor of GSH synthesis. In conclusion, DV2 infection could reduce host intracellular GSH concentration and benefited from this process. Supplemental GSH could inhibit viral production, indicating GSH might be valuable in the prevention and treatment of DV2 infection.

摘要

还原型谷胱甘肽(GSH)是最强大的细胞内抗氧化剂,也参与病毒感染。登革病毒(DV)感染的发病机制尚未完全阐明。本研究调查了DV2型感染与宿主细胞内GSH含量之间的关系。结果显示,DV2感染导致细胞内GSH减少,进而引起核因子κB(NF-κB)激活并增加DV2产生。补充GSH可显著抑制NF-κB激活,导致HepG2细胞中DV2产生减少。此外,在用GSH合成抑制剂丁硫氨酸亚砜胺(BSO)处理的HepG2细胞中,观察到NF-κB活性升高和DV2产生增加。总之,DV2感染可降低宿主细胞内GSH浓度并从中获益。补充GSH可抑制病毒产生,表明GSH可能在DV2感染的预防和治疗中具有重要价值。

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