Inhibition of curcumin on influenza A virus infection and influenzal pneumonia via oxidative stress, TLR2/4, p38/JNK MAPK and NF-κB pathways.
Identifieur interne : 000298 ( PubMed/Corpus ); précédent : 000297; suivant : 000299Inhibition of curcumin on influenza A virus infection and influenzal pneumonia via oxidative stress, TLR2/4, p38/JNK MAPK and NF-κB pathways.
Auteurs : Jianping Dai ; Liming Gu ; Yun Su ; Qianwen Wang ; Ying Zhao ; Xiaoxua Chen ; Huixiong Deng ; Weizhong Li ; Gefei Wang ; Kangsheng LiSource :
- International immunopharmacology [ 1878-1705 ] ; 2018.
English descriptors
- KwdEn :
- A549 Cells, Animals, Anti-Inflammatory Agents, Non-Steroidal, Curcumin (therapeutic use), Dogs, Female, Humans, Influenza A virus (physiology), Influenza, Human (drug therapy), Influenza, Human (immunology), JNK Mitogen-Activated Protein Kinases (metabolism), Madin Darby Canine Kidney Cells, Male, Mice, Mice, Inbred C57BL, NF-E2-Related Factor 2 (genetics), NF-E2-Related Factor 2 (metabolism), Orthomyxoviridae Infections (drug therapy), Orthomyxoviridae Infections (immunology), Oxidative Stress, Pneumonia (drug therapy), Pneumonia (immunology), RNA, Small Interfering (genetics), Signal Transduction (drug effects), Toll-Like Receptor 2 (metabolism), Toll-Like Receptor 4 (metabolism), Transcription Factor RelA (metabolism), Virus Replication (drug effects), p38 Mitogen-Activated Protein Kinases (metabolism).
- MESH :
- chemical , genetics : NF-E2-Related Factor 2, RNA, Small Interfering.
- chemical , metabolism : JNK Mitogen-Activated Protein Kinases, NF-E2-Related Factor 2, Toll-Like Receptor 2, Toll-Like Receptor 4, Transcription Factor RelA, p38 Mitogen-Activated Protein Kinases.
- chemical , therapeutic use : Curcumin.
- chemical : Anti-Inflammatory Agents, Non-Steroidal.
- drug effects : Signal Transduction, Virus Replication.
- drug therapy : Influenza, Human, Orthomyxoviridae Infections, Pneumonia.
- immunology : Influenza, Human, Orthomyxoviridae Infections, Pneumonia.
- physiology : Influenza A virus.
- A549 Cells, Animals, Dogs, Female, Humans, Madin Darby Canine Kidney Cells, Male, Mice, Mice, Inbred C57BL, Oxidative Stress.
Abstract
Oxidative stress, Nrf2-HO-1 and TLR-MAPK/NF-κB signaling pathways have been proved to be involved in influenza A virus (IAV) replication and influenzal pneumonia. In the previous studies, we have performed several high-throughput drug screenings based on the TLR pathways. In the present study, through plaque inhibition test, luciferase reporter assay, TCID50, qRT-PCR, western blotting, ELISA and siRNA assays, we investigated the effect and mechanism of action of curcumin against IAV infection in vitro and in vivo. The results showed that curcumin could directly inactivate IAV, blocked IAV adsorption and inhibited IAV proliferation. As for the underlying mechanisms, we found that curcumin could significantly inhibit IAV-induced oxidative stress, increased Nrf2, HO-1, NQO1, GSTA3 and IFN-β production, and suppressed IAV-induced activation of TLR2/4/7, Akt, p38/JNK MAPK and NF-κB pathways. Suppression of Nrf2 via siRNA significantly abolished the stimulatory effect of curcumin on HO-1, NQO1, GSTA3 and IFN-β production and meanwhile blocked the inhibitory effect of curcumin on IAV M2 production. Oxidant H2O2 and TLR2/4, p38/JNK and NF-κB agonists could significantly antagonize the anti-IAV activity of curcumin in vitro. Additionally, curcumin significantly increased the survival rate of mice, reduced lung index, inflammatory cytokines and lung IAV titer, and finally improved pulmonary histopathological changes after IAV infection. In conclusion, curcumin can directly inactivate IAV, inhibits IAV adsorption and replication; and its inhibition on IAV replication may be via activating Nrf2 signal and inhibiting IAV-induced activation of TLR2/4, p38/JNK MAPK and NF-κB pathways.
DOI: 10.1016/j.intimp.2017.11.009
PubMed: 29153953
Links to Exploration step
pubmed:29153953Le document en format XML
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Electronic address: daijpedu2008@163.com.</nlm:affiliation></affiliation></author><author><name sortKey="Gu, Liming" sort="Gu, Liming" uniqKey="Gu L" first="Liming" last="Gu">Liming Gu</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Su, Yun" sort="Su, Yun" uniqKey="Su Y" first="Yun" last="Su">Yun Su</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Qianwen" sort="Wang, Qianwen" uniqKey="Wang Q" first="Qianwen" last="Wang">Qianwen Wang</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, 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, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Xiaoxua" sort="Chen, Xiaoxua" uniqKey="Chen X" first="Xiaoxua" last="Chen">Xiaoxua Chen</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Deng, Huixiong" sort="Deng, Huixiong" uniqKey="Deng H" first="Huixiong" last="Deng">Huixiong Deng</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Weizhong" sort="Li, Weizhong" uniqKey="Li W" first="Weizhong" last="Li">Weizhong Li</name><affiliation><nlm:affiliation>Department of Veterinary Medicine, University of Maryland, College Park, Virginia-Maryland Regional College of Veterinary Medicine, 159 College Park Rd, MD 20742, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Gefei" sort="Wang, Gefei" uniqKey="Wang G" first="Gefei" last="Wang">Gefei Wang</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Kangsheng" sort="Li, Kangsheng" uniqKey="Li K" first="Kangsheng" last="Li">Kangsheng Li</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2018">2018</date><idno type="RBID">pubmed:29153953</idno><idno type="pmid">29153953</idno><idno type="doi">10.1016/j.intimp.2017.11.009</idno><idno type="wicri:Area/PubMed/Corpus">000298</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000298</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Inhibition of curcumin on influenza A virus infection and influenzal pneumonia via oxidative stress, TLR2/4, p38/JNK MAPK and NF-κB pathways.</title><author><name sortKey="Dai, Jianping" sort="Dai, Jianping" uniqKey="Dai J" first="Jianping" last="Dai">Jianping Dai</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China. Electronic address: daijpedu2008@163.com.</nlm:affiliation></affiliation></author><author><name sortKey="Gu, Liming" sort="Gu, Liming" uniqKey="Gu L" first="Liming" last="Gu">Liming Gu</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Su, Yun" sort="Su, Yun" uniqKey="Su Y" first="Yun" last="Su">Yun Su</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Qianwen" sort="Wang, Qianwen" uniqKey="Wang Q" first="Qianwen" last="Wang">Qianwen Wang</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, 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, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Xiaoxua" sort="Chen, Xiaoxua" uniqKey="Chen X" first="Xiaoxua" last="Chen">Xiaoxua Chen</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Deng, Huixiong" sort="Deng, Huixiong" uniqKey="Deng H" first="Huixiong" last="Deng">Huixiong Deng</name><affiliation><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Weizhong" sort="Li, Weizhong" uniqKey="Li W" first="Weizhong" 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type="abstract" xml:lang="en">Oxidative stress, Nrf2-HO-1 and TLR-MAPK/NF-κB signaling pathways have been proved to be involved in influenza A virus (IAV) replication and influenzal pneumonia. In the previous studies, we have performed several high-throughput drug screenings based on the TLR pathways. In the present study, through plaque inhibition test, luciferase reporter assay, TCID<sub>50</sub>, qRT-PCR, western blotting, ELISA and siRNA assays, we investigated the effect and mechanism of action of curcumin against IAV infection in vitro and in vivo. The results showed that curcumin could directly inactivate IAV, blocked IAV adsorption and inhibited IAV proliferation. As for the underlying mechanisms, we found that curcumin could significantly inhibit IAV-induced oxidative stress, increased Nrf2, HO-1, NQO1, GSTA3 and IFN-β production, and suppressed IAV-induced activation of TLR2/4/7, Akt, p38/JNK MAPK and NF-κB pathways. Suppression of Nrf2 via siRNA significantly abolished the stimulatory effect of curcumin on HO-1, NQO1, GSTA3 and IFN-β production and meanwhile blocked the inhibitory effect of curcumin on IAV M2 production. Oxidant H<sub>2</sub>O<sub>2</sub> and TLR2/4, p38/JNK and NF-κB agonists could significantly antagonize the anti-IAV activity of curcumin in vitro. Additionally, curcumin significantly increased the survival rate of mice, reduced lung index, inflammatory cytokines and lung IAV titer, and finally improved pulmonary histopathological changes after IAV infection. In conclusion, curcumin can directly inactivate IAV, inhibits IAV adsorption and replication; and its inhibition on IAV replication may be via activating Nrf2 signal and inhibiting IAV-induced activation of TLR2/4, p38/JNK MAPK and NF-κB pathways.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29153953</PMID><DateCompleted><Year>2018</Year><Month>07</Month><Day>27</Day></DateCompleted><DateRevised><Year>2018</Year><Month>07</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-1705</ISSN><JournalIssue CitedMedium="Internet"><Volume>54</Volume><PubDate><Year>2018</Year><Month>Jan</Month></PubDate></JournalIssue><Title>International immunopharmacology</Title><ISOAbbreviation>Int. Immunopharmacol.</ISOAbbreviation></Journal><ArticleTitle>Inhibition of curcumin on influenza A virus infection and influenzal pneumonia via oxidative stress, TLR2/4, p38/JNK MAPK and NF-κB pathways.</ArticleTitle><Pagination><MedlinePgn>177-187</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S1567-5769(17)30429-0</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.intimp.2017.11.009</ELocationID><Abstract><AbstractText>Oxidative stress, Nrf2-HO-1 and TLR-MAPK/NF-κB signaling pathways have been proved to be involved in influenza A virus (IAV) replication and influenzal pneumonia. In the previous studies, we have performed several high-throughput drug screenings based on the TLR pathways. In the present study, through plaque inhibition test, luciferase reporter assay, TCID<sub>50</sub>, qRT-PCR, western blotting, ELISA and siRNA assays, we investigated the effect and mechanism of action of curcumin against IAV infection in vitro and in vivo. The results showed that curcumin could directly inactivate IAV, blocked IAV adsorption and inhibited IAV proliferation. As for the underlying mechanisms, we found that curcumin could significantly inhibit IAV-induced oxidative stress, increased Nrf2, HO-1, NQO1, GSTA3 and IFN-β production, and suppressed IAV-induced activation of TLR2/4/7, Akt, p38/JNK MAPK and NF-κB pathways. Suppression of Nrf2 via siRNA significantly abolished the stimulatory effect of curcumin on HO-1, NQO1, GSTA3 and IFN-β production and meanwhile blocked the inhibitory effect of curcumin on IAV M2 production. Oxidant H<sub>2</sub>O<sub>2</sub> and TLR2/4, p38/JNK and NF-κB agonists could significantly antagonize the anti-IAV activity of curcumin in vitro. Additionally, curcumin significantly increased the survival rate of mice, reduced lung index, inflammatory cytokines and lung IAV titer, and finally improved pulmonary histopathological changes after IAV infection. In conclusion, curcumin can directly inactivate IAV, inhibits IAV adsorption and replication; and its inhibition on IAV replication may be via activating Nrf2 signal and inhibiting IAV-induced activation of TLR2/4, p38/JNK MAPK and NF-κB pathways.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dai</LastName><ForeName>Jianping</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China. Electronic address: daijpedu2008@163.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>Liming</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, 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, 22 Xingling Rd, Shantou 515041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Qianwen</ForeName><Initials>Q</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, 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, 22 Xingling Rd, Shantou 515041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xiaoxua</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Deng</LastName><ForeName>Huixiong</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Weizhong</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Department of Veterinary Medicine, University of Maryland, College Park, Virginia-Maryland Regional College of Veterinary Medicine, 159 College Park Rd, MD 20742, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Gefei</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Kangsheng</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>11</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Int Immunopharmacol</MedlineTA><NlmUniqueID>100965259</NlmUniqueID><ISSNLinking>1567-5769</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000894">Anti-Inflammatory Agents, Non-Steroidal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051267">NF-E2-Related Factor 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495635">NFE2L2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C498143">RELA protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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UI="D048051" MajorTopicYN="N">p38 Mitogen-Activated Protein Kinases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Curcumin</Keyword><Keyword MajorTopicYN="N">Influenza A virus</Keyword><Keyword MajorTopicYN="N">MAPK, NF-κB</Keyword><Keyword MajorTopicYN="N">Nrf2</Keyword><Keyword MajorTopicYN="N">TLRs</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>09</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>10</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>11</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>11</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2018</Year><Month>7</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>11</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">29153953</ArticleId><ArticleId IdType="pii">S1567-5769(17)30429-0</ArticleId><ArticleId IdType="doi">10.1016/j.intimp.2017.11.009</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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