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经典猪瘟病毒在猪脐静脉内皮细胞中诱导氧化应激。

Classical swine fever virus induces oxidative stress in swine umbilical vein endothelial cells.

作者信息

He Lei, Zhang Yanming, Fang Yanqin, Liang Wulong, Lin Jihui, Cheng Min

机构信息

College of Veterinary Medicine, Northwest A & F University, Yangling, Shaanxi, 712100, P.R. China.

Animal Disease and Public Security Academician Workstation of Henan province, The Key Lab of Animal Disease and Public security, Henan University of Science and Technology, Luoyang, 471003, P.R. China.

出版信息

BMC Vet Res. 2014 Dec 2;10:279. doi: 10.1186/s12917-014-0279-3.

DOI:10.1186/s12917-014-0279-3
PMID:25439655
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4270048/
Abstract

BACKGROUND

Classical swine fever virus (CSFV) infection causes significant losses of pigs, which is characterized by hemorrhage, disseminated intravascular coagulation and leucopenia. The swine vascular endothelial cell is a primary target cell for CSFV. The aim of this study was to determine the role of CSFV infection in inducing oxidative stress (OS) in vascular endothelial cells.

RESULTS

We demonstrated that CSFV infection induced oxidative stress in swine umbilical vein endothelial cells (SUVECs), characterized by the induction of reactive oxygen species (ROS) production and the elevations of porcine antioxidant proteins thioredoxin (Trx), peroxiredoxin-6 (PRDX-6) and heme oxygenase-1 (HO-1) expression. Furthermore, cyclooxygenase-2 (COX-2), a pro-inflammatory protein related to oxidative stress, was up-regulated while anti-inflammatory protein peroxisome proliferator-activated receptor-γ (PPAR-γ), an important mediator in vascular functional regulation, was down-regulated in the CSFV infected cells. In addition, antioxidants showed significant inhibitory effects on the CSFV replication, indicating a close relationship between CSFV replication and OS induced in the host cells.

CONCLUSIONS

Our results indicated that CSFV infection induced oxidative stress in SUVECs. These findings provide novel information on the mechanism by which CSFV can alter intracellular events associated with the viral infection.

摘要

背景

经典猪瘟病毒(CSFV)感染会给猪造成重大损失,其特征为出血、弥散性血管内凝血和白细胞减少。猪血管内皮细胞是CSFV的主要靶细胞。本研究的目的是确定CSFV感染在诱导血管内皮细胞氧化应激(OS)中的作用。

结果

我们证明CSFV感染可诱导猪脐静脉内皮细胞(SUVECs)产生氧化应激,其特征为活性氧(ROS)生成增加以及猪抗氧化蛋白硫氧还蛋白(Trx)、过氧化物酶-6(PRDX-6)和血红素加氧酶-1(HO-1)表达升高。此外,与氧化应激相关的促炎蛋白环氧化酶-2(COX-2)在CSFV感染的细胞中上调,而血管功能调节中的重要介质抗炎蛋白过氧化物酶体增殖物激活受体-γ(PPAR-γ)下调。此外,抗氧化剂对CSFV复制具有显著抑制作用,表明CSFV复制与宿主细胞中诱导的OS之间存在密切关系。

结论

我们的结果表明CSFV感染可诱导SUVECs产生氧化应激。这些发现为CSFV改变与病毒感染相关的细胞内事件的机制提供了新信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/45dadc9d88e0/12917_2014_279_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/a42955b09046/12917_2014_279_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/9ba176dac793/12917_2014_279_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/184343b62bfa/12917_2014_279_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/b5fa6d3c9ab9/12917_2014_279_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/3b8bb8c8638b/12917_2014_279_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/be091f789c76/12917_2014_279_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/45dadc9d88e0/12917_2014_279_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/a42955b09046/12917_2014_279_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/9ba176dac793/12917_2014_279_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/184343b62bfa/12917_2014_279_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/b5fa6d3c9ab9/12917_2014_279_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/3b8bb8c8638b/12917_2014_279_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/be091f789c76/12917_2014_279_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c300/4270048/45dadc9d88e0/12917_2014_279_Fig7_HTML.jpg

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