Anti-influenza A virus activity of rhein through regulating oxidative stress, TLR4, Akt, MAPK, and NF-κB signal pathways.
Identifieur interne : 000281 ( PubMed/Corpus ); précédent : 000280; suivant : 000282Anti-influenza A virus activity of rhein through regulating oxidative stress, TLR4, Akt, MAPK, and NF-κB signal pathways.
Auteurs : Qian-Wen Wang ; Yun Su ; Jiang-Tao Sheng ; Li-Ming Gu ; Ying Zhao ; Xiao-Xuan Chen ; Cheng Chen ; Wei-Zhong Li ; Kang-Sheng Li ; Jian-Ping DaiSource :
- PloS one [ 1932-6203 ] ; 2018.
English descriptors
- KwdEn :
- A549 Cells, Animals, Anthraquinones (pharmacology), Antiviral Agents (pharmacology), Cytokines (biosynthesis), Dogs, Female, Humans, Influenza A Virus, H1N1 Subtype (drug effects), Influenza A Virus, H1N1 Subtype (pathogenicity), Influenza A Virus, H1N1 Subtype (physiology), Lung (drug effects), Lung (pathology), MAP Kinase Signaling System (drug effects), Madin Darby Canine Kidney Cells, Male, Matrix Metalloproteinases (biosynthesis), Mice, Mice, Inbred C57BL, NF-kappa B (metabolism), Orthomyxoviridae Infections (drug therapy), Orthomyxoviridae Infections (metabolism), Orthomyxoviridae Infections (virology), Oxidative Stress (drug effects), Pneumonia, Viral (drug therapy), Pneumonia, Viral (pathology), Pneumonia, Viral (physiopathology), Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (drug effects), Toll-Like Receptor 4 (metabolism), Virus Attachment (drug effects), Virus Replication (drug effects).
- MESH :
- chemical , biosynthesis : Cytokines, Matrix Metalloproteinases.
- chemical , metabolism : NF-kappa B, Proto-Oncogene Proteins c-akt, Toll-Like Receptor 4.
- chemical , pharmacology : Anthraquinones, Antiviral Agents.
- drug effects : Influenza A Virus, H1N1 Subtype, Lung, MAP Kinase Signaling System, Oxidative Stress, Signal Transduction, Virus Attachment, Virus Replication.
- drug therapy : Orthomyxoviridae Infections, Pneumonia, Viral.
- metabolism : Orthomyxoviridae Infections.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- pathology : Lung, Pneumonia, Viral.
- physiology : Influenza A Virus, H1N1 Subtype.
- physiopathology : Pneumonia, Viral.
- virology : Orthomyxoviridae Infections.
- A549 Cells, Animals, Dogs, Female, Humans, Madin Darby Canine Kidney Cells, Male, Mice, Mice, Inbred C57BL.
Abstract
Rhein, an anthraquinone compound existing in many traditional herbal medicines, has anti-inflammatory, antioxidant, antitumor, antiviral, hepatoprotective, and nephroprotective activities, but its anti-influenza A virus (IAV) activity is ambiguous. In the present study, through plaque inhibition assay, time-of-addition assay, antioxidant assay, qRT-PCR, ELISA, and western blotting assays, we investigated the anti-IAV effect and mechanism of action of rhein in vitro and in vivo. The results showed that rhein could significantly inhibit IAV adsorption and replication, decrease IAV-induced oxidative stress, activations of TLR4, Akt, p38, JNK MAPK, and NF-κB pathways, and production of inflammatory cytokines and matrix metalloproteinases in vitro. Oxidant H2O2 and agonists of TLR4, Akt, p38/JNK and IKK/NF-κB could significantly antagonize the inhibitory effects of rhein on IAV-induced cytopathic effect (CPE) and IAV replication. Through an in vivo test in mice, we also found that rhein could significantly improve the survival rate, lung index, pulmonary cytokines, and pulmonary histopathological changes. Rhein also significantly decreased pulmonary viral load at a high dose. In conclusion, rhein can inhibit IAV adsorption and replication, and the mechanism of action to inhibit IAV replication may be due to its ability to suppress IAV-induced oxidative stress and activations of TLR4, Akt, p38, JNK MAPK, and NF-κB signal pathways.
DOI: 10.1371/journal.pone.0191793
PubMed: 29385192
Links to Exploration step
pubmed:29385192Le document en format XML
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Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Gu, Li Ming" sort="Gu, Li Ming" uniqKey="Gu L" first="Li-Ming" last="Gu">Li-Ming Gu</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhao, Ying" sort="Zhao, Ying" uniqKey="Zhao Y" first="Ying" last="Zhao">Ying Zhao</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Xiao Xuan" sort="Chen, Xiao Xuan" uniqKey="Chen X" first="Xiao-Xuan" last="Chen">Xiao-Xuan Chen</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Cheng" sort="Chen, Cheng" uniqKey="Chen C" first="Cheng" last="Chen">Cheng Chen</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Wei Zhong" sort="Li, Wei Zhong" uniqKey="Li W" first="Wei-Zhong" last="Li">Wei-Zhong Li</name><affiliation><nlm:affiliation>Department of Veterinary Medicine, University of Maryland, College Park, Maryland, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Kang Sheng" sort="Li, Kang Sheng" uniqKey="Li K" first="Kang-Sheng" last="Li">Kang-Sheng Li</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Dai, Jian Ping" sort="Dai, Jian Ping" uniqKey="Dai J" first="Jian-Ping" last="Dai">Jian-Ping 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Ying" uniqKey="Zhao Y" first="Ying" last="Zhao">Ying Zhao</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Xiao Xuan" sort="Chen, Xiao Xuan" uniqKey="Chen X" first="Xiao-Xuan" last="Chen">Xiao-Xuan Chen</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Cheng" sort="Chen, Cheng" uniqKey="Chen C" first="Cheng" last="Chen">Cheng Chen</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Wei Zhong" sort="Li, Wei Zhong" uniqKey="Li W" first="Wei-Zhong" last="Li">Wei-Zhong Li</name><affiliation><nlm:affiliation>Department of Veterinary Medicine, University of Maryland, College Park, Maryland, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Kang Sheng" sort="Li, Kang Sheng" uniqKey="Li K" first="Kang-Sheng" last="Li">Kang-Sheng Li</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author><author><name sortKey="Dai, Jian Ping" sort="Dai, Jian Ping" uniqKey="Dai J" first="Jian-Ping" last="Dai">Jian-Ping Dai</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</nlm:affiliation></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A549 Cells</term><term>Animals</term><term>Anthraquinones (pharmacology)</term><term>Antiviral Agents (pharmacology)</term><term>Cytokines (biosynthesis)</term><term>Dogs</term><term>Female</term><term>Humans</term><term>Influenza A Virus, H1N1 Subtype (drug effects)</term><term>Influenza A Virus, H1N1 Subtype (pathogenicity)</term><term>Influenza A Virus, H1N1 Subtype (physiology)</term><term>Lung (drug effects)</term><term>Lung (pathology)</term><term>MAP Kinase Signaling System (drug effects)</term><term>Madin Darby Canine Kidney Cells</term><term>Male</term><term>Matrix Metalloproteinases (biosynthesis)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>NF-kappa B (metabolism)</term><term>Orthomyxoviridae Infections (drug therapy)</term><term>Orthomyxoviridae Infections (metabolism)</term><term>Orthomyxoviridae Infections (virology)</term><term>Oxidative Stress (drug effects)</term><term>Pneumonia, Viral (drug therapy)</term><term>Pneumonia, Viral (pathology)</term><term>Pneumonia, Viral (physiopathology)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Signal Transduction (drug effects)</term><term>Toll-Like Receptor 4 (metabolism)</term><term>Virus Attachment (drug effects)</term><term>Virus Replication (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Cytokines</term><term>Matrix Metalloproteinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>NF-kappa B</term><term>Proto-Oncogene Proteins c-akt</term><term>Toll-Like Receptor 4</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anthraquinones</term><term>Antiviral Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term><term>Lung</term><term>MAP Kinase Signaling System</term><term>Oxidative Stress</term><term>Signal Transduction</term><term>Virus Attachment</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Orthomyxoviridae Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" xml:lang="en"><term>A549 Cells</term><term>Animals</term><term>Dogs</term><term>Female</term><term>Humans</term><term>Madin Darby Canine Kidney Cells</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Rhein, an anthraquinone compound existing in many traditional herbal medicines, has anti-inflammatory, antioxidant, antitumor, antiviral, hepatoprotective, and nephroprotective activities, but its anti-influenza A virus (IAV) activity is ambiguous. In the present study, through plaque inhibition assay, time-of-addition assay, antioxidant assay, qRT-PCR, ELISA, and western blotting assays, we investigated the anti-IAV effect and mechanism of action of rhein in vitro and in vivo. The results showed that rhein could significantly inhibit IAV adsorption and replication, decrease IAV-induced oxidative stress, activations of TLR4, Akt, p38, JNK MAPK, and NF-κB pathways, and production of inflammatory cytokines and matrix metalloproteinases in vitro. Oxidant H2O2 and agonists of TLR4, Akt, p38/JNK and IKK/NF-κB could significantly antagonize the inhibitory effects of rhein on IAV-induced cytopathic effect (CPE) and IAV replication. Through an in vivo test in mice, we also found that rhein could significantly improve the survival rate, lung index, pulmonary cytokines, and pulmonary histopathological changes. Rhein also significantly decreased pulmonary viral load at a high dose. In conclusion, rhein can inhibit IAV adsorption and replication, and the mechanism of action to inhibit IAV replication may be due to its ability to suppress IAV-induced oxidative stress and activations of TLR4, Akt, p38, JNK MAPK, and NF-κB signal pathways.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29385192</PMID><DateCompleted><Year>2018</Year><Month>03</Month><Day>12</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>13</Volume><Issue>1</Issue><PubDate><Year>2018</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Anti-influenza A virus activity of rhein through regulating oxidative stress, TLR4, Akt, MAPK, and NF-κB signal pathways.</ArticleTitle><Pagination><MedlinePgn>e0191793</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0191793</ELocationID><Abstract><AbstractText>Rhein, an anthraquinone compound existing in many traditional herbal medicines, has anti-inflammatory, antioxidant, antitumor, antiviral, hepatoprotective, and nephroprotective activities, but its anti-influenza A virus (IAV) activity is ambiguous. In the present study, through plaque inhibition assay, time-of-addition assay, antioxidant assay, qRT-PCR, ELISA, and western blotting assays, we investigated the anti-IAV effect and mechanism of action of rhein in vitro and in vivo. The results showed that rhein could significantly inhibit IAV adsorption and replication, decrease IAV-induced oxidative stress, activations of TLR4, Akt, p38, JNK MAPK, and NF-κB pathways, and production of inflammatory cytokines and matrix metalloproteinases in vitro. Oxidant H2O2 and agonists of TLR4, Akt, p38/JNK and IKK/NF-κB could significantly antagonize the inhibitory effects of rhein on IAV-induced cytopathic effect (CPE) and IAV replication. Through an in vivo test in mice, we also found that rhein could significantly improve the survival rate, lung index, pulmonary cytokines, and pulmonary histopathological changes. Rhein also significantly decreased pulmonary viral load at a high dose. In conclusion, rhein can inhibit IAV adsorption and replication, and the mechanism of action to inhibit IAV replication may be due to its ability to suppress IAV-induced oxidative stress and activations of TLR4, Akt, p38, JNK MAPK, and NF-κB signal pathways.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Qian-Wen</ForeName><Initials>QW</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Su</LastName><ForeName>Yun</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sheng</LastName><ForeName>Jiang-Tao</ForeName><Initials>JT</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>Li-Ming</ForeName><Initials>LM</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Ying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xiao-Xuan</ForeName><Initials>XX</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Cheng</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Wei-Zhong</ForeName><Initials>WZ</Initials><AffiliationInfo><Affiliation>Department of Veterinary Medicine, University of Maryland, College Park, Maryland, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Kang-Sheng</ForeName><Initials>KS</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dai</LastName><ForeName>Jian-Ping</ForeName><Initials>JP</Initials><Identifier Source="ORCID">0000-0002-8304-8207</Identifier><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>01</Month><Day>31</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000880">Anthraquinones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral 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