Article(id=1259888467211858805, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1259888457367806489, articleNumber=null, orderNo=null, doi=10.13343/j.cnki.wsxb.20250684, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1757088000000, receivedDateStr=2025-09-06, revisedDate=null, revisedDateStr=null, acceptedDate=1767542400000, acceptedDateStr=2026-01-05, onlineDate=1778310418178, onlineDateStr=2026-05-09, pubDate=1777824000000, pubDateStr=2026-05-04, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1778310418178, onlineIssueDateStr=2026-05-09, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1778310418178, creator=13701087609, updateTime=1778310418178, updator=13701087609, issue=Issue{id=1259888457367806489, tenantId=1146029695717560320, journalId=1192105938417971205, year='2026', volume='66', issue='5', pageStart='2031', pageEnd='2556', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=0, articleOrder=1, issueType=-1, specialIssue=null, createTime=1778310415832, creator=13701087609, updateTime=1778320153326, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1259929299465921482, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1259888457367806489, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1259929299465921483, tenantId=1146029695717560320, journalId=1192105938417971205, issueId=1259888457367806489, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=2031, endPage=2047, ext={EN=ArticleExt(id=1259888469673915277, articleId=1259888467211858805, tenantId=1146029695717560320, journalId=1192105938417971205, language=EN, title=Research progress in the role of oxidative stress in porcine enteric coronavirus infection and related therapies, columnId=1192149543727808575, journalTitle=Acta Microbiologica Sinica, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Porcine enteric coronaviruses (PECs) include porcine epidemic diarrhea virus (PEDV), transmissible gastroenteritis virus (TGEV), and porcine deltacoronavirus (PDCoV). Infections with PECs can cause severe diarrhea in pigs, particularly newborn piglets, resulting in high mortality rates and posing a serious threat and economic loss to the global swine industry. Such infections induce oxidative stress to activate various transcription factors and alter their transcriptional pathways, thereby affecting cellular metabolism and the viral life cycle. This leads to cellular dysfunction and further promotes viral replication, forming a vicious cycle. The oxidative stress associated with PECs is considered one of the potential common pathogenic mechanisms. This review summarizes the information about the oxidative stress induced by infections with PECs and emphasizes that antioxidant strategies represent one of the effective approaches to counteract such infections.

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猪肠道冠状病毒(porcine enteric coronaviruses, PECs)包括猪流行性腹泻病毒(porcine epidemic diarrhea virus, PEDV)、传染性胃肠炎病毒(transmissible gastroenteritis virus, TGEV)和猪δ冠状病毒(porcine deltacoronavirus, PDCoV)。PECs感染会导致猪(尤其是新生仔猪)出现严重腹泻，具有高致死率，给全球养猪业带来重大威胁并造成经济损失。PECs感染会引发氧化应激，进而激活多种转录因子，改变其转录途径，影响细胞代谢和病毒的生命周期，最终导致细胞功能障碍，并进一步促进病毒增殖，形成恶性循环。PECs感染增加的氧化应激被视为潜在的共同病因之一。本文综述了PECs感染引起的相关氧化应激信息，并强调抗氧化是应对PECs感染的有效策略之一。

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Animals, 2022, 12(4): 458., articleTitle=The aqueous leaf extract of M. oleifera inhibits PEDV replication through suppressing oxidative stress-mediated apoptosis, refAbstract=null), Reference(id=1259928555450975211, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, doi=null, pmid=null, pmcid=null, year=2022, volume=14, issue=2, pageStart=402, pageEnd=null, url=null, language=null, rfNumber=[138], rfOrder=138, authorNames=Liu Y, Wang X, Wang J, Zhang JL, Duan C, Wang JF, journalName=Viruses, refType=null, unstructuredReference=Liu Y, Wang X, Wang J, Zhang JL, Duan C, Wang JF. Ergosterol peroxide inhibits porcine epidemic diarrhea virus infection in vero cells by suppressing ROS generation and p53 activation[J]. Viruses, 2022, 14(2): 402., articleTitle=Ergosterol peroxide inhibits porcine epidemic diarrhea virus infection in vero cells by suppressing ROS generation and p53 activation, refAbstract=null), Reference(id=1259928555648107502, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, doi=null, pmid=null, pmcid=null, year=2024, volume=20, issue=null, pageStart=288, pageEnd=null, url=null, language=null, rfNumber=[139], rfOrder=139, authorNames=Wang JR, Zeng XY, Gou JJ, Zhu XJ, Yin DD, Yin L, Shen XH, Dai Y, Pan XC, journalName=BMC Veterinary Research, refType=null, unstructuredReference=Wang JR, Zeng XY, Gou JJ, Zhu XJ, Yin DD, Yin L, Shen XH, Dai Y, Pan XC. Antiviral activity of luteolin against porcine epidemic diarrhea virus in silico and in vitro [J]. BMC Veterinary Research, 2024, 20: 288., articleTitle=Antiviral activity of luteolin against porcine epidemic diarrhea virus in silico and in vitro, refAbstract=null), Reference(id=1259928555916542960, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, doi=null, pmid=null, pmcid=null, year=2025, volume=208, issue=null, pageStart=107957, pageEnd=null, url=null, language=null, rfNumber=[140], rfOrder=140, authorNames=Zhi YP, Ren YP, Xia XM, Tian Q, Meng YS, Tao SY, journalName=Microbial Pathogenesis, refType=null, unstructuredReference=Zhi YP, Ren YP, Xia XM, Tian Q, Meng YS, Tao SY. Chrysin inhibits PEDV replication by antagonizing apoptosis via the ROS/JNK/p53 axis[J]. Microbial Pathogenesis, 2025, 208: 107957., articleTitle=Chrysin inhibits PEDV replication by antagonizing apoptosis via the ROS/JNK/p53 axis, refAbstract=null), Reference(id=1259928556067537907, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, doi=null, pmid=null, pmcid=null, year=2025, volume=15, issue=9, pageStart=1207, pageEnd=null, url=null, language=null, rfNumber=[141], rfOrder=141, authorNames=Sun YW, Wang LY, Ma KK, Shen MM, Liu JY, Zhang YJ, Sun LM, journalName=Animals, refType=null, unstructuredReference=Sun YW, Wang LY, Ma KK, Shen MM, Liu JY, Zhang YJ, Sun LM. Antiviral activity of 1-deoxynojirimycin extracts of mulberry leaves against porcine epidemic diarrhea virus[J]. Animals, 2025, 15(9): 1207., articleTitle=Antiviral activity of 1-deoxynojirimycin extracts of mulberry leaves against porcine epidemic diarrhea virus, refAbstract=null)], funds=[Fund(id=1259928424701935659, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, awardId=32360893, language=EN, fundingSource=The Regional Science Found Project of the National Natural Science Foundation of China(32360893), fundOrder=null, country=null), Fund(id=1259928425557573694, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, awardId=32360893, language=CN, fundingSource=国家自然科学基金地区科学基金(32360893), fundOrder=null, country=null), Fund(id=1259928427965104203, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, awardId=YDBK2021-15, language=EN, fundingSource=The Yan’an University Doctoral Research Initiation Project(YDBK2021-15), fundOrder=null, country=null), Fund(id=1259928430209056855, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, awardId=YDBK2021-15, language=CN, fundingSource=延安大学博士科研启动项目(YDBK2021-15), fundOrder=null, country=null)], companyList=[AuthorCompany(id=1259928376207393440, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, xref=1., ext=[AuthorCompanyExt(id=1259928376215782049, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, companyId=1259928376207393440, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=^1.School of Physical Education, Yan’an University, Yan’an, Shaanxi, China), AuthorCompanyExt(id=1259928376228364963, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, companyId=1259928376207393440, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=^1.延安大学 体育学院，陕西 延安)]), AuthorCompany(id=1259928376542937769, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, xref=2., ext=[AuthorCompanyExt(id=1259928376551326379, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, companyId=1259928376542937769, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=^2.Division of Science and Technology, Yan’an University, Yan’an, Shaanxi, China), AuthorCompanyExt(id=1259928376719098541, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, companyId=1259928376542937769, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=^2.延安大学 科学技术处，陕西 延安)])], figs=[ArticleFig(id=1259928407467541397, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, language=EN, label=Figure 1, caption=The relationship between TGEV infection and oxidative stress. During the infection process of TGEV, the p53 and ROS-mediated AIF pathway and caspase-dependent pathway jointly participate in the apoptosis process induced by TGEV; TGEV activates the production of ROS, induces apoptosis of Paneth cells and loss of Notch factors, affecting the normal self-renewal and differentiation of Lgr5+ stem cells; Abnormal differentiation of Lgr5+ stem cells into goblet cells results in the secretion of sialylated mucus, which provides favorable conditions for TGEV infection and exacerbates intestinal damage and viral replication; The ROS generation induced by TGEV may activate p38 MAPK and phosphorylation of p53, and p53 may partially regulate the generation of ROS; The accumulation of ROS leads to changes in mitochondrial outer membrane permeability (MOMP), release of cytochrome c, and subsequently activates Caspase-3, initiating the intrinsic apoptotic pathway; TGEV infection may upregulate Keap1 expression, inhibit Nrf2 and its downstream antioxidant genes (Ho-1, NQO1), resulting in accumulation of oxidative stress and induction of apoptosis; TGEV also inhibits oxidative stress induced by mitochondrial damage through upregulation of DJ-1 protein. This process can inhibit apoptosis, promote selective autophagy degradation of damaged mitochondria, and enhance viral infection., figureFileSmall=3ECXP50P5OM77qBKLwZ1pA==, figureFileBig=49cytn0MR2qMqUbtDtxaQA==, tableContent=null), ArticleFig(id=1259928409111708579, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, language=CN, label=图1, caption=TGEV感染与氧化应激的关系, figureFileSmall=3ECXP50P5OM77qBKLwZ1pA==, figureFileBig=49cytn0MR2qMqUbtDtxaQA==, tableContent=null), ArticleFig(id=1259928413331178448, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, language=EN, label=Figure 2, caption=The relationship between PEDV infection and oxidative stress. PEDV infection induces mitochondrial metabolic disorder through the CREB3L1/miR-34c/COX1 axis, increases mitochondrial ROS accumulation, and stimulates mitochondrial autophagy; PEDV controls endoplasmic reticulum to perturb its redox homeostasis through the PERK-CHOP-ERO1α-ROS axis in favor of its replication. In PEDV-infected piglets, RORγ/NRF2 regulates the transcriptional levels of key genes of mevalonate (MVA) through epigenetic mechanisms, blocking the biosynthesis of GPx4 and reducing catalase (CAT), resulting in lipid peroxidation in the piglet’s liver. PEDV induces DNA damage response through the ROS-ATM signaling pathway, thereby promoting its early replication, or through oxidative stress, induced by the PERK and IRE1 pathways, promoting endoplasmic reticulum stress and cell autophagy., figureFileSmall=6gB1JUuHjDs+v9ikVTOO+g==, figureFileBig=tfoZGrioTEMd2aES6RM0UQ==, tableContent=null), ArticleFig(id=1259928414589469659, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, language=CN, label=图2, caption=PEDV感染与氧化应激的关系, figureFileSmall=6gB1JUuHjDs+v9ikVTOO+g==, figureFileBig=tfoZGrioTEMd2aES6RM0UQ==, tableContent=null), ArticleFig(id=1259928416149750755, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, language=EN, label=Figure 3, caption=The relationship between PDCoV infection and oxidative stress. PDCoV infection can trigger autophagy in cells. Oxidative stress further promotes autophagy activation by generating ROS, interfering with the host immune signaling pathways, thereby facilitating viral replication. PDCoV infection can induce oxidative stress in host cells and affect the expression of mitochondrial antiviral signaling protein (MAVS) and the phosphorylation level of interferon regulatory factor-3 (IRF-3), thereby interfering with the innate immune response. SIRT5 interacts with and desuccinylates the PDCoV membrane (M) protein. This modification activates the ATM pathway to induce the ubiquitination of PEX5 and recruits p62 to initiate selective pexophagy, which disrupts the function of peroxisomes and increases ROS levels, inhibits the production of type I and type III interferons, and thereby promotes viral replication; PDCoV infection inhibits the Nrf2 pathway, reduces the levels of HO-1 and NQO1, leading to oxidative stress, promoting viral replication, and inducing tissue or cell damage., figureFileSmall=zRn7JpwqOegurjsQa6vU9w==, figureFileBig=aPoRfPRlACihkoovfrZWPg==, tableContent=null), ArticleFig(id=1259928418704081910, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, language=CN, label=图3, caption=PDCoV感染与氧化应激的关系, figureFileSmall=zRn7JpwqOegurjsQa6vU9w==, figureFileBig=aPoRfPRlACihkoovfrZWPg==, tableContent=null), ArticleFig(id=1259928421623316487, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, language=EN, label=Table 1, caption=

Antioxidant drugs with potential therapeutic effects on PECs and their possible mechanisms of action

, figureFileSmall=null, figureFileBig=null, tableContent=

Antioxidant drugs	Virus type	Antiviral mechanism	References
Selenomethionine	Porcine deltacoronavirus (PDCoV)	Enhance cellular antioxidant capacity; activate the Nrf2 signaling pathway, reduce ROS levels, and alleviate intestinal damage	[37-38,65]
N-acetylcysteine	Porcine epidemic diarrhea virus (PEDV)	Reduced H2O2 levels and alleviate intestinal damage. Enhance the spleen’s antioxidant, anti-inflammatory, immune, and tissue repair capabilities	[123-124]
Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA)	Porcine epidemic diarrhea virus (PEDV)	Reduce ER stress, enhance antioxidant capacity, and lower inflammation levels	[132]
(+)-catechin	Transmissible gastroenteritis virus (TGEV)	Reduce ROS production	[133]
Polygonum cillinerve polysaccharide	Transmissible gastroenteritis virus (TGEV)	Reduce ROS production and alleviate apoptosis	[134]
Eugenol	Transmissible gastroenteritis virus (TGEV)	Activate the Keap1-Nrf2-ARE signaling pathway to reduce ROS production and apoptosis; inhibit ROS/NLRP3/GSDMD-dependent pyroptosis to alleviate intestinal injury	[40,135]
All-trans retinoic acid	Transmissible gastroenteritis virus (TGEV)	Inhibition of ROS-mediated p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway reduces apoptosis	[136]
Aqueous leaf extract	Porcine epidemic diarrhea virus (PEDV)	Interfere with the replication phase of the viral life cycle, suppress oxidative stress, and mitigate apoptosis	[137]
Ergosterol peroxide	Porcine epidemic diarrhea virus (PEDV)	By suppressing ROS production and activating the p53 pathway, PEDV replication is inhibited	[138]
Luteolin	Porcine epidemic diarrhea virus (PEDV)	By targeting the substrate-binding site of the PEDV Mpro protein, it inhibits the enzyme’s activity, thereby disrupting PEDV replication, suppressing inflammatory responses, and activating the Nrf2/HO-1 antioxidant pathway	[139]
Chrysin	Porcine epidemic diarrhea virus (PEDV)	Poplar extract inhibits PEDV replication through the ROS/JNK/p53 axis	[140]
L-deoxynojirimycin Extracts of mulberry leaves	Porcine epidemic diarrhea virus (PEDV)	l-deoxynojirimycin can reduce ROS production associated with PEDV infection, thereby decreasing MDA levels, enhancing GSH-Px activity, and alleviating the inflammatory response in host cells triggered by PEDV invasion	[141]

), ArticleFig(id=1259928422860636184, tenantId=1146029695717560320, journalId=1192105938417971205, articleId=1259888467211858805, language=CN, label=表1, caption=

对PECs具有潜在治疗效果的抗氧化药物及其可能的作用机制

, figureFileSmall=null, figureFileBig=null, tableContent=

Antioxidant drugs	Virus type	Antiviral mechanism	References
Selenomethionine	Porcine deltacoronavirus (PDCoV)	Enhance cellular antioxidant capacity; activate the Nrf2 signaling pathway, reduce ROS levels, and alleviate intestinal damage	[37-38,65]
N-acetylcysteine	Porcine epidemic diarrhea virus (PEDV)	Reduced H2O2 levels and alleviate intestinal damage. Enhance the spleen’s antioxidant, anti-inflammatory, immune, and tissue repair capabilities	[123-124]
Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA)	Porcine epidemic diarrhea virus (PEDV)	Reduce ER stress, enhance antioxidant capacity, and lower inflammation levels	[132]
(+)-catechin	Transmissible gastroenteritis virus (TGEV)	Reduce ROS production	[133]
Polygonum cillinerve polysaccharide	Transmissible gastroenteritis virus (TGEV)	Reduce ROS production and alleviate apoptosis	[134]
Eugenol	Transmissible gastroenteritis virus (TGEV)	Activate the Keap1-Nrf2-ARE signaling pathway to reduce ROS production and apoptosis; inhibit ROS/NLRP3/GSDMD-dependent pyroptosis to alleviate intestinal injury	[40,135]
All-trans retinoic acid	Transmissible gastroenteritis virus (TGEV)	Inhibition of ROS-mediated p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway reduces apoptosis	[136]
Aqueous leaf extract	Porcine epidemic diarrhea virus (PEDV)	Interfere with the replication phase of the viral life cycle, suppress oxidative stress, and mitigate apoptosis	[137]
Ergosterol peroxide	Porcine epidemic diarrhea virus (PEDV)	By suppressing ROS production and activating the p53 pathway, PEDV replication is inhibited	[138]
Luteolin	Porcine epidemic diarrhea virus (PEDV)	By targeting the substrate-binding site of the PEDV Mpro protein, it inhibits the enzyme’s activity, thereby disrupting PEDV replication, suppressing inflammatory responses, and activating the Nrf2/HO-1 antioxidant pathway	[139]
Chrysin	Porcine epidemic diarrhea virus (PEDV)	Poplar extract inhibits PEDV replication through the ROS/JNK/p53 axis	[140]
L-deoxynojirimycin Extracts of mulberry leaves	Porcine epidemic diarrhea virus (PEDV)	l-deoxynojirimycin can reduce ROS production associated with PEDV infection, thereby decreasing MDA levels, enhancing GSH-Px activity, and alleviating the inflammatory response in host cells triggered by PEDV invasion	[141]

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