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 : 000991 ( Main/Exploration ); précédent : 000990; suivant : 000992Inhibition 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 [République populaire de Chine] ; Liming Gu [République populaire de Chine] ; Yun Su [République populaire de Chine] ; Qianwen Wang [République populaire de Chine] ; Ying Zhao [République populaire de Chine] ; Xiaoxua Chen [République populaire de Chine] ; Huixiong Deng [République populaire de Chine] ; Weizhong Li [États-Unis] ; Gefei Wang [République populaire de Chine] ; Kangsheng Li [République populaire de Chine]Source :
- International immunopharmacology [ 1878-1705 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux, Anti-inflammatoires non stéroïdiens, Cellules A549, Cellules rénales canines Madin-Darby, Chiens, Curcumine (usage thérapeutique), Facteur de transcription RelA (métabolisme), Facteur-2 apparenté à NF-E2 (génétique), Facteur-2 apparenté à NF-E2 (métabolisme), Femelle, Grippe humaine (immunologie), Grippe humaine (traitement médicamenteux), Humains, Infections à Orthomyxoviridae (immunologie), Infections à Orthomyxoviridae (traitement médicamenteux), JNK Mitogen-Activated Protein Kinases (métabolisme), Mâle, Petit ARN interférent (génétique), Pneumopathie infectieuse (immunologie), Pneumopathie infectieuse (traitement médicamenteux), Récepteur de type Toll-2 (métabolisme), Récepteur de type Toll-4 (métabolisme), Réplication virale (), Souris, Souris de lignée C57BL, Stress oxydatif, Transduction du signal (), Virus de la grippe A (physiologie), p38 Mitogen-Activated Protein Kinases (métabolisme).
- MESH :
- génétique : Facteur-2 apparenté à NF-E2, Petit ARN interférent.
- immunologie : Grippe humaine, Infections à Orthomyxoviridae, Pneumopathie infectieuse.
- métabolisme : Facteur de transcription RelA, Facteur-2 apparenté à NF-E2, JNK Mitogen-Activated Protein Kinases, Récepteur de type Toll-2, Récepteur de type Toll-4, p38 Mitogen-Activated Protein Kinases.
- physiologie : Virus de la grippe A.
- traitement médicamenteux : Grippe humaine, Infections à Orthomyxoviridae, Pneumopathie infectieuse.
- usage thérapeutique : Curcumine.
- Animaux, Anti-inflammatoires non stéroïdiens, Cellules A549, Cellules rénales canines Madin-Darby, Chiens, Femelle, Humains, Mâle, Réplication virale, Souris, Souris de lignée C57BL, Stress oxydatif, Transduction du signal.
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
Affiliations:
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Le document en format XML
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wicri:level="4"><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><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Veterinary Medicine, University of Maryland, College Park, Virginia-Maryland Regional College of Veterinary Medicine, 159 College Park Rd, MD 20742</wicri:regionArea><placeName><region type="state">Maryland</region><settlement type="city">College Park (Maryland)</settlement></placeName><orgName type="university">Université du Maryland</orgName></affiliation></author><author><name sortKey="Wang, Gefei" sort="Wang, Gefei" uniqKey="Wang G" first="Gefei" last="Wang">Gefei Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation><country xml:lang="fr">République 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pathways.</title><author><name sortKey="Dai, Jianping" sort="Dai, Jianping" uniqKey="Dai J" first="Jianping" last="Dai">Jianping Dai</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China. 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Su</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041</wicri:regionArea><wicri:noRegion>Shantou 515041</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Qianwen" sort="Wang, Qianwen" uniqKey="Wang Q" first="Qianwen" last="Wang">Qianwen Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041</wicri:regionArea><wicri:noRegion>Shantou 515041</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Ying" sort="Zhao, Ying" uniqKey="Zhao Y" first="Ying" last="Zhao">Ying Zhao</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041</wicri:regionArea><wicri:noRegion>Shantou 515041</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Xiaoxua" sort="Chen, Xiaoxua" uniqKey="Chen X" first="Xiaoxua" last="Chen">Xiaoxua Chen</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041</wicri:regionArea><wicri:noRegion>Shantou 515041</wicri:noRegion></affiliation></author><author><name sortKey="Deng, Huixiong" sort="Deng, Huixiong" uniqKey="Deng H" first="Huixiong" last="Deng">Huixiong Deng</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041</wicri:regionArea><wicri:noRegion>Shantou 515041</wicri:noRegion></affiliation></author><author><name sortKey="Li, Weizhong" sort="Li, Weizhong" uniqKey="Li W" first="Weizhong" last="Li">Weizhong Li</name><affiliation wicri:level="4"><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><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Veterinary Medicine, University of Maryland, College Park, Virginia-Maryland Regional College of Veterinary Medicine, 159 College Park Rd, MD 20742</wicri:regionArea><placeName><region type="state">Maryland</region><settlement type="city">College Park (Maryland)</settlement></placeName><orgName type="university">Université du Maryland</orgName></affiliation></author><author><name sortKey="Wang, Gefei" sort="Wang, Gefei" uniqKey="Wang G" first="Gefei" last="Wang">Gefei Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041</wicri:regionArea><wicri:noRegion>Shantou 515041</wicri:noRegion></affiliation></author><author><name sortKey="Li, Kangsheng" sort="Li, Kangsheng" uniqKey="Li K" first="Kangsheng" last="Li">Kangsheng Li</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Immunology, Shantou University Medical College, 22 Xingling Rd, Shantou 515041</wicri:regionArea><wicri:noRegion>Shantou 515041</wicri:noRegion></affiliation></author></analytic><series><title level="j">International immunopharmacology</title><idno type="eISSN">1878-1705</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>Anti-Inflammatory Agents, Non-Steroidal</term><term>Curcumin (therapeutic use)</term><term>Dogs</term><term>Female</term><term>Humans</term><term>Influenza A virus (physiology)</term><term>Influenza, Human (drug therapy)</term><term>Influenza, Human (immunology)</term><term>JNK Mitogen-Activated Protein Kinases (metabolism)</term><term>Madin Darby Canine Kidney Cells</term><term>Male</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>NF-E2-Related Factor 2 (genetics)</term><term>NF-E2-Related Factor 2 (metabolism)</term><term>Orthomyxoviridae Infections (drug therapy)</term><term>Orthomyxoviridae Infections (immunology)</term><term>Oxidative Stress</term><term>Pneumonia (drug therapy)</term><term>Pneumonia (immunology)</term><term>RNA, Small Interfering (genetics)</term><term>Signal Transduction (drug effects)</term><term>Toll-Like Receptor 2 (metabolism)</term><term>Toll-Like Receptor 4 (metabolism)</term><term>Transcription Factor RelA (metabolism)</term><term>Virus Replication (drug effects)</term><term>p38 Mitogen-Activated Protein Kinases (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anti-inflammatoires non stéroïdiens</term><term>Cellules A549</term><term>Cellules rénales canines Madin-Darby</term><term>Chiens</term><term>Curcumine (usage thérapeutique)</term><term>Facteur de transcription RelA (métabolisme)</term><term>Facteur-2 apparenté à NF-E2 (génétique)</term><term>Facteur-2 apparenté à NF-E2 (métabolisme)</term><term>Femelle</term><term>Grippe humaine (immunologie)</term><term>Grippe humaine (traitement médicamenteux)</term><term>Humains</term><term>Infections à Orthomyxoviridae (immunologie)</term><term>Infections à Orthomyxoviridae (traitement médicamenteux)</term><term>JNK Mitogen-Activated Protein Kinases (métabolisme)</term><term>Mâle</term><term>Petit ARN interférent (génétique)</term><term>Pneumopathie infectieuse (immunologie)</term><term>Pneumopathie infectieuse (traitement médicamenteux)</term><term>Récepteur de type Toll-2 (métabolisme)</term><term>Récepteur de type Toll-4 (métabolisme)</term><term>Réplication virale ()</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Stress oxydatif</term><term>Transduction du signal ()</term><term>Virus de la grippe A (physiologie)</term><term>p38 Mitogen-Activated Protein Kinases (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>NF-E2-Related Factor 2</term><term>RNA, Small Interfering</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>JNK Mitogen-Activated Protein Kinases</term><term>NF-E2-Related Factor 2</term><term>Toll-Like Receptor 2</term><term>Toll-Like Receptor 4</term><term>Transcription Factor RelA</term><term>p38 Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Curcumin</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Signal Transduction</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Influenza, Human</term><term>Orthomyxoviridae Infections</term><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur-2 apparenté à NF-E2</term><term>Petit ARN interférent</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Grippe humaine</term><term>Infections à Orthomyxoviridae</term><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza, Human</term><term>Orthomyxoviridae Infections</term><term>Pneumonia</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de transcription RelA</term><term>Facteur-2 apparenté à NF-E2</term><term>JNK Mitogen-Activated Protein Kinases</term><term>Récepteur de type Toll-2</term><term>Récepteur de type Toll-4</term><term>p38 Mitogen-Activated Protein Kinases</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Grippe humaine</term><term>Infections à Orthomyxoviridae</term><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Curcumine</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><term>Oxidative Stress</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Anti-inflammatoires non stéroïdiens</term><term>Cellules A549</term><term>Cellules rénales canines Madin-Darby</term><term>Chiens</term><term>Femelle</term><term>Humains</term><term>Mâle</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Stress oxydatif</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div 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><affiliations><list><country><li>République populaire de Chine</li><li>États-Unis</li></country><region><li>Maryland</li></region><settlement><li>College Park (Maryland)</li></settlement><orgName><li>Université du Maryland</li></orgName></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Dai, Jianping" sort="Dai, Jianping" uniqKey="Dai J" first="Jianping" last="Dai">Jianping Dai</name></noRegion><name sortKey="Chen, Xiaoxua" sort="Chen, Xiaoxua" uniqKey="Chen X" first="Xiaoxua" last="Chen">Xiaoxua Chen</name><name sortKey="Deng, Huixiong" sort="Deng, Huixiong" uniqKey="Deng H" first="Huixiong" last="Deng">Huixiong Deng</name><name sortKey="Gu, Liming" sort="Gu, Liming" uniqKey="Gu L" first="Liming" last="Gu">Liming Gu</name><name sortKey="Li, Kangsheng" sort="Li, Kangsheng" uniqKey="Li K" first="Kangsheng" last="Li">Kangsheng Li</name><name sortKey="Su, Yun" sort="Su, Yun" uniqKey="Su Y" first="Yun" last="Su">Yun Su</name><name sortKey="Wang, Gefei" sort="Wang, Gefei" uniqKey="Wang G" first="Gefei" last="Wang">Gefei Wang</name><name sortKey="Wang, Qianwen" sort="Wang, Qianwen" uniqKey="Wang Q" first="Qianwen" last="Wang">Qianwen Wang</name><name sortKey="Zhao, Ying" sort="Zhao, Ying" uniqKey="Zhao Y" first="Ying" last="Zhao">Ying Zhao</name></country><country name="États-Unis"><region name="Maryland"><name sortKey="Li, Weizhong" sort="Li, Weizhong" uniqKey="Li W" first="Weizhong" last="Li">Weizhong Li</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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