Drug screening for autophagy inhibitors based on the dissociation of Beclin1-Bcl2 complex using BiFC technique and mechanism of eugenol on anti-influenza A virus activity.
Identifieur interne : 000531 ( PubMed/Checkpoint ); précédent : 000530; suivant : 000532Drug screening for autophagy inhibitors based on the dissociation of Beclin1-Bcl2 complex using BiFC technique and mechanism of eugenol on anti-influenza A virus activity.
Auteurs : Jian-Ping Dai [République populaire de Chine] ; Xiang-Feng Zhao ; Jun Zeng ; Qian-Ying Wan ; Jia-Cai Yang ; Wei-Zhong Li ; Xiao-Xuan Chen ; Ge-Fei Wang ; Kang-Sheng LiSource :
- PloS one [ 1932-6203 ] ; 2013.
Descripteurs français
- KwdFr :
- MESH :
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacology : Antiviral Agents, Drugs, Chinese Herbal, Eugenol.
- chemistry : Syzygium.
- drug effects : Autophagy, Influenza A virus.
- methods : Drug Evaluation, Preclinical.
- Cell Line, Humans.
Abstract
Autophagy is involved in many human diseases, such as cancer, cardiovascular disease and virus infection, including human immunodeficiency virus (HIV), hepatitis C virus (HCV), influenza A virus (IAV) and coxsackievirus B3/B4 (CVB3/B4), so a drug screening model targeting autophagy may be very useful for the therapy of these diseases. In our study, we established a drug screening model based on the inhibition of the dissociation of Beclin1-Bcl2 heterodimer, an important negative regulator of autophagy, using bimolecular fluorescence complementation (BiFC) technique for developing novel autophagy inhibitors and anti-IAV agents. From 86 examples of traditional Chinese medicines, we found Syzygium aromaticum L. had the best activity. We then determined the anti-autophagy and anti-IAV activity of eugenol, the major active compound of Syzygium aromaticum L., and explored its mechanism of action. Eugenol could inhibit autophagy and IAV replication, inhibited the activation of ERK, p38MAPK and IKK/NF-κB signal pathways and antagonized the effects of the activators of these pathways. Eugenol also ameliorated the oxidative stress and inhibited the expressions of autophagic genes. We speculated that the mechanism underlying might be that eugenol inhibited the oxidative stress and the activation of ERK1/2, p38MAPK and IKK/NF-κB pathways, subsequently inhibited the dissociation of Beclin1-Bcl2 heterodimer and autophagy, and finally impaired IAV replication. These results might conversely display the reasonableness of the design of our screening model. In conclusion, we have established a drug screening model for developing novel autophagy inhibitor, and find eugenol as a promising inhibitor for autophagy and IAV infection.
DOI: 10.1371/journal.pone.0061026
PubMed: 23613775
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Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, People's Republic of China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong</wicri:regionArea><wicri:noRegion>Guangdong</wicri:noRegion></affiliation></author><author><name sortKey="Zhao, Xiang Feng" sort="Zhao, Xiang Feng" uniqKey="Zhao X" first="Xiang-Feng" last="Zhao">Xiang-Feng Zhao</name></author><author><name sortKey="Zeng, Jun" sort="Zeng, Jun" uniqKey="Zeng J" first="Jun" last="Zeng">Jun Zeng</name></author><author><name sortKey="Wan, Qian Ying" sort="Wan, Qian Ying" uniqKey="Wan Q" first="Qian-Ying" last="Wan">Qian-Ying Wan</name></author><author><name sortKey="Yang, Jia Cai" sort="Yang, Jia Cai" uniqKey="Yang J" first="Jia-Cai" last="Yang">Jia-Cai Yang</name></author><author><name sortKey="Li, Wei Zhong" sort="Li, Wei Zhong" uniqKey="Li W" first="Wei-Zhong" last="Li">Wei-Zhong Li</name></author><author><name sortKey="Chen, Xiao Xuan" sort="Chen, Xiao Xuan" uniqKey="Chen X" first="Xiao-Xuan" last="Chen">Xiao-Xuan Chen</name></author><author><name sortKey="Wang, Ge Fei" sort="Wang, Ge Fei" uniqKey="Wang G" first="Ge-Fei" last="Wang">Ge-Fei Wang</name></author><author><name sortKey="Li, Kang Sheng" sort="Li, Kang Sheng" uniqKey="Li K" first="Kang-Sheng" last="Li">Kang-Sheng Li</name></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiviral Agents (pharmacology)</term><term>Autophagy (drug effects)</term><term>Cell Line</term><term>Drug Evaluation, Preclinical (methods)</term><term>Drugs, Chinese Herbal (pharmacology)</term><term>Eugenol (pharmacology)</term><term>Humans</term><term>Influenza A virus (drug effects)</term><term>Syzygium (chemistry)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antiviraux (pharmacologie)</term><term>Autophagie ()</term><term>Eugénol (pharmacologie)</term><term>Humains</term><term>Lignée cellulaire</term><term>Médicaments issus de plantes chinoises (pharmacologie)</term><term>Syzygium ()</term><term>Virus de la grippe A ()</term><term>Évaluation préclinique de médicament ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiviral Agents</term><term>Drugs, Chinese Herbal</term><term>Eugenol</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Syzygium</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Drug Evaluation, Preclinical</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antiviraux</term><term>Eugénol</term><term>Médicaments issus de plantes chinoises</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term><term>Humains</term><term>Lignée cellulaire</term><term>Syzygium</term><term>Virus de la grippe A</term><term>Évaluation préclinique de médicament</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy is involved in many human diseases, such as cancer, cardiovascular disease and virus infection, including human immunodeficiency virus (HIV), hepatitis C virus (HCV), influenza A virus (IAV) and coxsackievirus B3/B4 (CVB3/B4), so a drug screening model targeting autophagy may be very useful for the therapy of these diseases. In our study, we established a drug screening model based on the inhibition of the dissociation of Beclin1-Bcl2 heterodimer, an important negative regulator of autophagy, using bimolecular fluorescence complementation (BiFC) technique for developing novel autophagy inhibitors and anti-IAV agents. From 86 examples of traditional Chinese medicines, we found Syzygium aromaticum L. had the best activity. We then determined the anti-autophagy and anti-IAV activity of eugenol, the major active compound of Syzygium aromaticum L., and explored its mechanism of action. Eugenol could inhibit autophagy and IAV replication, inhibited the activation of ERK, p38MAPK and IKK/NF-κB signal pathways and antagonized the effects of the activators of these pathways. Eugenol also ameliorated the oxidative stress and inhibited the expressions of autophagic genes. We speculated that the mechanism underlying might be that eugenol inhibited the oxidative stress and the activation of ERK1/2, p38MAPK and IKK/NF-κB pathways, subsequently inhibited the dissociation of Beclin1-Bcl2 heterodimer and autophagy, and finally impaired IAV replication. These results might conversely display the reasonableness of the design of our screening model. In conclusion, we have established a drug screening model for developing novel autophagy inhibitor, and find eugenol as a promising inhibitor for autophagy and IAV infection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23613775</PMID><DateCompleted><Year>2013</Year><Month>11</Month><Day>14</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>4</Issue><PubDate><Year>2013</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Drug screening for autophagy inhibitors based on the dissociation of Beclin1-Bcl2 complex using BiFC technique and mechanism of eugenol on anti-influenza A virus activity.</ArticleTitle><Pagination><MedlinePgn>e61026</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0061026</ELocationID><Abstract><AbstractText>Autophagy is involved in many human diseases, such as cancer, cardiovascular disease and virus infection, including human immunodeficiency virus (HIV), hepatitis C virus (HCV), influenza A virus (IAV) and coxsackievirus B3/B4 (CVB3/B4), so a drug screening model targeting autophagy may be very useful for the therapy of these diseases. In our study, we established a drug screening model based on the inhibition of the dissociation of Beclin1-Bcl2 heterodimer, an important negative regulator of autophagy, using bimolecular fluorescence complementation (BiFC) technique for developing novel autophagy inhibitors and anti-IAV agents. From 86 examples of traditional Chinese medicines, we found Syzygium aromaticum L. had the best activity. We then determined the anti-autophagy and anti-IAV activity of eugenol, the major active compound of Syzygium aromaticum L., and explored its mechanism of action. Eugenol could inhibit autophagy and IAV replication, inhibited the activation of ERK, p38MAPK and IKK/NF-κB signal pathways and antagonized the effects of the activators of these pathways. Eugenol also ameliorated the oxidative stress and inhibited the expressions of autophagic genes. We speculated that the mechanism underlying might be that eugenol inhibited the oxidative stress and the activation of ERK1/2, p38MAPK and IKK/NF-κB pathways, subsequently inhibited the dissociation of Beclin1-Bcl2 heterodimer and autophagy, and finally impaired IAV replication. These results might conversely display the reasonableness of the design of our screening model. In conclusion, we have established a drug screening model for developing novel autophagy inhibitor, and find eugenol as a promising inhibitor for autophagy and IAV infection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dai</LastName><ForeName>Jian-Ping</ForeName><Initials>JP</Initials><AffiliationInfo><Affiliation>Department of Microbiology and Immunology, Shantou University Medical College, Shantou, Guangdong, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhao</LastName><ForeName>Xiang-Feng</ForeName><Initials>XF</Initials></Author><Author ValidYN="Y"><LastName>Zeng</LastName><ForeName>Jun</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Wan</LastName><ForeName>Qian-Ying</ForeName><Initials>QY</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Jia-Cai</ForeName><Initials>JC</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Wei-Zhong</ForeName><Initials>WZ</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Xiao-Xuan</ForeName><Initials>XX</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Ge-Fei</ForeName><Initials>GF</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Kang-Sheng</ForeName><Initials>KS</Initials></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>2013</Year><Month>04</Month><Day>16</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 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Fei" sort="Wang, Ge Fei" uniqKey="Wang G" first="Ge-Fei" last="Wang">Ge-Fei Wang</name><name sortKey="Yang, Jia Cai" sort="Yang, Jia Cai" uniqKey="Yang J" first="Jia-Cai" last="Yang">Jia-Cai Yang</name><name sortKey="Zeng, Jun" sort="Zeng, Jun" uniqKey="Zeng J" first="Jun" last="Zeng">Jun Zeng</name><name sortKey="Zhao, Xiang Feng" sort="Zhao, Xiang Feng" uniqKey="Zhao X" first="Xiang-Feng" last="Zhao">Xiang-Feng Zhao</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Dai, Jian Ping" sort="Dai, Jian Ping" uniqKey="Dai J" first="Jian-Ping" last="Dai">Jian-Ping Dai</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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