Anti-influenza A virus activity of rhein through regulating oxidative stress, TLR4, Akt, MAPK, and NF-κB signal pathways.
Identifieur interne : 000A22 ( Main/Exploration ); précédent : 000A21; suivant : 000A23Anti-influenza A virus activity of rhein through regulating oxidative stress, TLR4, Akt, MAPK, and NF-κB signal pathways.
Auteurs : Qian-Wen Wang [République populaire de Chine] ; Yun Su [République populaire de Chine] ; Jiang-Tao Sheng [République populaire de Chine] ; Li-Ming Gu [République populaire de Chine] ; Ying Zhao [République populaire de Chine] ; Xiao-Xuan Chen [République populaire de Chine] ; Cheng Chen [République populaire de Chine] ; Wei-Zhong Li [États-Unis] ; Kang-Sheng Li [République populaire de Chine] ; Jian-Ping Dai [République populaire de Chine]Source :
- PloS one [ 1932-6203 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux, Anthraquinones (pharmacologie), Antiviraux (pharmacologie), Attachement viral (), Cellules A549, Cellules rénales canines Madin-Darby, Chiens, Cytokines (biosynthèse), Facteur de transcription NF-kappa B (métabolisme), Femelle, Humains, Infections à Orthomyxoviridae (métabolisme), Infections à Orthomyxoviridae (traitement médicamenteux), Infections à Orthomyxoviridae (virologie), Matrix metalloproteinases (biosynthèse), Mâle, Pneumopathie virale (anatomopathologie), Pneumopathie virale (physiopathologie), Pneumopathie virale (traitement médicamenteux), Poumon (), Poumon (anatomopathologie), Protéines proto-oncogènes c-akt (métabolisme), Récepteur de type Toll-4 (métabolisme), Réplication virale (), Souris, Souris de lignée C57BL, Sous-type H1N1 du virus de la grippe A (), Sous-type H1N1 du virus de la grippe A (pathogénicité), Sous-type H1N1 du virus de la grippe A (physiologie), Stress oxydatif (), Système de signalisation des MAP kinases (), Transduction du signal ().
- MESH :
- anatomopathologie : Pneumopathie virale, Poumon.
- biosynthèse : Cytokines, Matrix metalloproteinases.
- métabolisme : Facteur de transcription NF-kappa B, Infections à Orthomyxoviridae, Protéines proto-oncogènes c-akt, Récepteur de type Toll-4.
- pathogénicité : Sous-type H1N1 du virus de la grippe A.
- pharmacologie : Anthraquinones, Antiviraux.
- physiologie : Sous-type H1N1 du virus de la grippe A.
- physiopathologie : Pneumopathie virale.
- traitement médicamenteux : Infections à Orthomyxoviridae, Pneumopathie virale.
- virologie : Infections à Orthomyxoviridae.
- Animaux, Attachement viral, Cellules A549, Cellules rénales canines Madin-Darby, Chiens, Femelle, Humains, Mâle, Poumon, Réplication virale, Souris, Souris de lignée C57BL, Sous-type H1N1 du virus de la grippe A, Stress oxydatif, Système de signalisation des MAP kinases, Transduction du signal.
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
Affiliations:
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Le document en format XML
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<author><name sortKey="Chen, Cheng" sort="Chen, Cheng" uniqKey="Chen C" first="Cheng" last="Chen">Cheng Chen</name>
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<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="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Anthraquinones (pharmacologie)</term>
<term>Antiviraux (pharmacologie)</term>
<term>Attachement viral ()</term>
<term>Cellules A549</term>
<term>Cellules rénales canines Madin-Darby</term>
<term>Chiens</term>
<term>Cytokines (biosynthèse)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Infections à Orthomyxoviridae (métabolisme)</term>
<term>Infections à Orthomyxoviridae (traitement médicamenteux)</term>
<term>Infections à Orthomyxoviridae (virologie)</term>
<term>Matrix metalloproteinases (biosynthèse)</term>
<term>Mâle</term>
<term>Pneumopathie virale (anatomopathologie)</term>
<term>Pneumopathie virale (physiopathologie)</term>
<term>Pneumopathie virale (traitement médicamenteux)</term>
<term>Poumon ()</term>
<term>Poumon (anatomopathologie)</term>
<term>Protéines proto-oncogènes c-akt (métabolisme)</term>
<term>Récepteur de type Toll-4 (métabolisme)</term>
<term>Réplication virale ()</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Sous-type H1N1 du virus de la grippe A ()</term>
<term>Sous-type H1N1 du virus de la grippe A (pathogénicité)</term>
<term>Sous-type H1N1 du virus de la grippe A (physiologie)</term>
<term>Stress oxydatif ()</term>
<term>Système de signalisation des MAP kinases ()</term>
<term>Transduction du signal ()</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="anatomopathologie" xml:lang="fr"><term>Pneumopathie virale</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Cytokines</term>
<term>Matrix metalloproteinases</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="métabolisme" xml:lang="fr"><term>Facteur de transcription NF-kappa B</term>
<term>Infections à Orthomyxoviridae</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Récepteur de type Toll-4</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term>
<term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anthraquinones</term>
<term>Antiviraux</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Sous-type H1N1 du virus de la grippe A</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Pneumopathie virale</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Pneumonia, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Infections à Orthomyxoviridae</term>
<term>Pneumopathie virale</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à Orthomyxoviridae</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>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Attachement viral</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>Poumon</term>
<term>Réplication virale</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
<term>Stress oxydatif</term>
<term>Système de signalisation des MAP kinases</term>
<term>Transduction du signal</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>
<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="Wang, Qian Wen" sort="Wang, Qian Wen" uniqKey="Wang Q" first="Qian-Wen" last="Wang">Qian-Wen Wang</name>
</noRegion>
<name sortKey="Chen, Cheng" sort="Chen, Cheng" uniqKey="Chen C" first="Cheng" last="Chen">Cheng Chen</name>
<name sortKey="Chen, Xiao Xuan" sort="Chen, Xiao Xuan" uniqKey="Chen X" first="Xiao-Xuan" last="Chen">Xiao-Xuan Chen</name>
<name sortKey="Dai, Jian Ping" sort="Dai, Jian Ping" uniqKey="Dai J" first="Jian-Ping" last="Dai">Jian-Ping Dai</name>
<name sortKey="Gu, Li Ming" sort="Gu, Li Ming" uniqKey="Gu L" first="Li-Ming" last="Gu">Li-Ming Gu</name>
<name sortKey="Li, Kang Sheng" sort="Li, Kang Sheng" uniqKey="Li K" first="Kang-Sheng" last="Li">Kang-Sheng Li</name>
<name sortKey="Sheng, Jiang Tao" sort="Sheng, Jiang Tao" uniqKey="Sheng J" first="Jiang-Tao" last="Sheng">Jiang-Tao Sheng</name>
<name sortKey="Su, Yun" sort="Su, Yun" uniqKey="Su Y" first="Yun" last="Su">Yun Su</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, Wei Zhong" sort="Li, Wei Zhong" uniqKey="Li W" first="Wei-Zhong" last="Li">Wei-Zhong Li</name>
</region>
</country>
</tree>
</affiliations>
</record>
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