Pinitol attenuates LPS-induced pneumonia in experimental animals: Possible role via inhibition of the TLR-4 and NF-κB/IκBα signaling cascade pathway.
Identifieur interne : 000083 ( Main/Exploration ); précédent : 000082; suivant : 000084Pinitol attenuates LPS-induced pneumonia in experimental animals: Possible role via inhibition of the TLR-4 and NF-κB/IκBα signaling cascade pathway.
Auteurs : Yingying Fan [République populaire de Chine] ; Jian Wang [République populaire de Chine] ; Zhihui Feng [République populaire de Chine] ; Ke Cao [République populaire de Chine] ; Hao Xu [République populaire de Chine] ; Jiankang Liu [République populaire de Chine]Source :
- Journal of biochemical and molecular toxicology [ 1099-0461 ] ; 2020.
Abstract
Pneumonia is a chronic disorder of the respiratory system associated with worsening quality of life and a significant economic burden. Pinitol, a plant cyclic polyol, has been documented for immune-inflammatory potential. The aim of present investigation was to evaluate the potential and possible mechanism of action of pinitol against lipopolysaccharide (LPS)-induced pneumonia in the experimental animal model. Pneumonia was induced in Sprague-Dawley rats by intratracheal administration of LPS (2 mg/kg). Animals were treated with either vehicle or dexamethasone or pinitol (5 or 10 or 20 mg/kg). Potential of pinitol against LPS-induced pulmonary insult was assessed based on behavioral, biochemical, molecular, and ultrastructural studies. Intratracheal instillation of LPS induced significant (P < .05) inflammatory infiltration in bronchoalveolar lavage fluid (BALF) and lung tissue reflected by elevated pleural effusion volume, lung edema, BALF polymorphonuclear leukocytes count and lung myeloperoxidase levels, which was attenuated by pinitol (10 and 20 mg/kg) administration. Pinitol also markedly (P < .05) inhibited LPS-induced alterations in electrocardiographic, hemodynamic changes, right ventricular, and lung function tests. The LPS-induced downregulated nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase-1 (HO-1), whereas upregulated transforming growth factor-β (TGF-β), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3), and inducible nitric oxide synthase (iNOs) lung messenger RNA expressions were significantly (P < .05) inhibited by pinitol. Western blot analysis suggested pinitol markedly (P < .05) decreased nuclear factor-κB (NF-κB), inhibitor of nuclear factor κB (IkBα), toll-like receptor 4 (TLR-4), and cyclooxygenase-II (COX-II) protein expressions in the lung. These findings were further supported by histological and ultrastructural analyses of lung tissue that show pinitol significantly (P < .05) ameliorates LPS-induced aberrations in lung tissue. In conclusion, pinitol attenuated LPS-induced pneumonia via inhibition of TLR-4 to downregulate the NF-κB/IκBα signaling cascade and thus ameliorated the production of proinflammatory cytokines (TNF-α, ILs, NLRP3, and TGF-β), inflammatory mediators (COX-II and iNOs) and elevated oxidative stress (Nrf-2 and HO-1).
DOI: 10.1002/jbt.22622
PubMed: 32926510
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Pinitol attenuates LPS-induced pneumonia in experimental animals: Possible role via inhibition of the TLR-4 and NF-κB/IκBα signaling cascade pathway.</title><author><name sortKey="Fan, Yingying" sort="Fan, Yingying" uniqKey="Fan Y" first="Yingying" last="Fan">Yingying Fan</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Jian" sort="Wang, Jian" uniqKey="Wang J" first="Jian" last="Wang">Jian Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Otolaryngology-Head and Neck Surgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Otolaryngology-Head and Neck Surgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Feng, Zhihui" sort="Feng, Zhihui" uniqKey="Feng Z" first="Zhihui" last="Feng">Zhihui Feng</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Ke" sort="Cao, Ke" uniqKey="Cao K" first="Ke" last="Cao">Ke Cao</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Hao" sort="Xu, Hao" uniqKey="Xu H" first="Hao" last="Xu">Hao Xu</name><affiliation wicri:level="1"><nlm:affiliation>Basic of Medical Science, Xi'an Medical University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Basic of Medical Science, Xi'an Medical University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Jiankang" sort="Liu, Jiankang" uniqKey="Liu J" first="Jiankang" last="Liu">Jiankang Liu</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32926510</idno><idno type="pmid">32926510</idno><idno type="doi">10.1002/jbt.22622</idno><idno type="wicri:Area/Main/Corpus">000050</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000050</idno><idno type="wicri:Area/Main/Curation">000050</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">000050</idno><idno type="wicri:Area/Main/Exploration">000050</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Pinitol attenuates LPS-induced pneumonia in experimental animals: Possible role via inhibition of the TLR-4 and NF-κB/IκBα signaling cascade pathway.</title><author><name sortKey="Fan, Yingying" sort="Fan, Yingying" uniqKey="Fan Y" first="Yingying" last="Fan">Yingying Fan</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Jian" sort="Wang, Jian" uniqKey="Wang J" first="Jian" last="Wang">Jian Wang</name><affiliation wicri:level="1"><nlm:affiliation>Department of Otolaryngology-Head and Neck Surgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Otolaryngology-Head and Neck Surgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Feng, Zhihui" sort="Feng, Zhihui" uniqKey="Feng Z" first="Zhihui" last="Feng">Zhihui Feng</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Cao, Ke" sort="Cao, Ke" uniqKey="Cao K" first="Ke" last="Cao">Ke Cao</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Xu, Hao" sort="Xu, Hao" uniqKey="Xu H" first="Hao" last="Xu">Hao Xu</name><affiliation wicri:level="1"><nlm:affiliation>Basic of Medical Science, Xi'an Medical University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Basic of Medical Science, Xi'an Medical University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author><author><name sortKey="Liu, Jiankang" sort="Liu, Jiankang" uniqKey="Liu J" first="Jiankang" last="Liu">Jiankang Liu</name><affiliation wicri:level="1"><nlm:affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi</wicri:regionArea><wicri:noRegion>Shaanxi</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of biochemical and molecular toxicology</title><idno type="eISSN">1099-0461</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pneumonia is a chronic disorder of the respiratory system associated with worsening quality of life and a significant economic burden. Pinitol, a plant cyclic polyol, has been documented for immune-inflammatory potential. The aim of present investigation was to evaluate the potential and possible mechanism of action of pinitol against lipopolysaccharide (LPS)-induced pneumonia in the experimental animal model. Pneumonia was induced in Sprague-Dawley rats by intratracheal administration of LPS (2 mg/kg). Animals were treated with either vehicle or dexamethasone or pinitol (5 or 10 or 20 mg/kg). Potential of pinitol against LPS-induced pulmonary insult was assessed based on behavioral, biochemical, molecular, and ultrastructural studies. Intratracheal instillation of LPS induced significant (P < .05) inflammatory infiltration in bronchoalveolar lavage fluid (BALF) and lung tissue reflected by elevated pleural effusion volume, lung edema, BALF polymorphonuclear leukocytes count and lung myeloperoxidase levels, which was attenuated by pinitol (10 and 20 mg/kg) administration. Pinitol also markedly (P < .05) inhibited LPS-induced alterations in electrocardiographic, hemodynamic changes, right ventricular, and lung function tests. The LPS-induced downregulated nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase-1 (HO-1), whereas upregulated transforming growth factor-β (TGF-β), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3), and inducible nitric oxide synthase (iNOs) lung messenger RNA expressions were significantly (P < .05) inhibited by pinitol. Western blot analysis suggested pinitol markedly (P < .05) decreased nuclear factor-κB (NF-κB), inhibitor of nuclear factor κB (IkBα), toll-like receptor 4 (TLR-4), and cyclooxygenase-II (COX-II) protein expressions in the lung. These findings were further supported by histological and ultrastructural analyses of lung tissue that show pinitol significantly (P < .05) ameliorates LPS-induced aberrations in lung tissue. In conclusion, pinitol attenuated LPS-induced pneumonia via inhibition of TLR-4 to downregulate the NF-κB/IκBα signaling cascade and thus ameliorated the production of proinflammatory cytokines (TNF-α, ILs, NLRP3, and TGF-β), inflammatory mediators (COX-II and iNOs) and elevated oxidative stress (Nrf-2 and HO-1).</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">32926510</PMID><DateRevised><Year>2020</Year><Month>09</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1099-0461</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2020</Year><Month>Sep</Month><Day>14</Day></PubDate></JournalIssue><Title>Journal of biochemical and molecular toxicology</Title><ISOAbbreviation>J Biochem Mol Toxicol</ISOAbbreviation></Journal><ArticleTitle>Pinitol attenuates LPS-induced pneumonia in experimental animals: Possible role via inhibition of the TLR-4 and NF-κB/IκBα signaling cascade pathway.</ArticleTitle><Pagination><MedlinePgn>e22622</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/jbt.22622</ELocationID><Abstract><AbstractText>Pneumonia is a chronic disorder of the respiratory system associated with worsening quality of life and a significant economic burden. Pinitol, a plant cyclic polyol, has been documented for immune-inflammatory potential. The aim of present investigation was to evaluate the potential and possible mechanism of action of pinitol against lipopolysaccharide (LPS)-induced pneumonia in the experimental animal model. Pneumonia was induced in Sprague-Dawley rats by intratracheal administration of LPS (2 mg/kg). Animals were treated with either vehicle or dexamethasone or pinitol (5 or 10 or 20 mg/kg). Potential of pinitol against LPS-induced pulmonary insult was assessed based on behavioral, biochemical, molecular, and ultrastructural studies. Intratracheal instillation of LPS induced significant (P < .05) inflammatory infiltration in bronchoalveolar lavage fluid (BALF) and lung tissue reflected by elevated pleural effusion volume, lung edema, BALF polymorphonuclear leukocytes count and lung myeloperoxidase levels, which was attenuated by pinitol (10 and 20 mg/kg) administration. Pinitol also markedly (P < .05) inhibited LPS-induced alterations in electrocardiographic, hemodynamic changes, right ventricular, and lung function tests. The LPS-induced downregulated nuclear factor erythroid 2-related factor 2 (Nrf-2) and heme oxygenase-1 (HO-1), whereas upregulated transforming growth factor-β (TGF-β), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3), and inducible nitric oxide synthase (iNOs) lung messenger RNA expressions were significantly (P < .05) inhibited by pinitol. Western blot analysis suggested pinitol markedly (P < .05) decreased nuclear factor-κB (NF-κB), inhibitor of nuclear factor κB (IkBα), toll-like receptor 4 (TLR-4), and cyclooxygenase-II (COX-II) protein expressions in the lung. These findings were further supported by histological and ultrastructural analyses of lung tissue that show pinitol significantly (P < .05) ameliorates LPS-induced aberrations in lung tissue. In conclusion, pinitol attenuated LPS-induced pneumonia via inhibition of TLR-4 to downregulate the NF-κB/IκBα signaling cascade and thus ameliorated the production of proinflammatory cytokines (TNF-α, ILs, NLRP3, and TGF-β), inflammatory mediators (COX-II and iNOs) and elevated oxidative stress (Nrf-2 and HO-1).</AbstractText><CopyrightInformation>© 2020 Wiley Periodicals LLC.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fan</LastName><ForeName>Yingying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Jian</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Otolaryngology-Head and Neck Surgery, Xijing Hospital, Air Force Medical University, Xi'an, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feng</LastName><ForeName>Zhihui</ForeName><Initials>Z</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cao</LastName><ForeName>Ke</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Hao</ForeName><Initials>H</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-6913-1154</Identifier><AffiliationInfo><Affiliation>Basic of Medical Science, Xi'an Medical University, Xi'an, Shaanxi, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Jiankang</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Key Laboratory of Biomedical Information Engineering of Ministry of Education, Center for Mitochondrial Biology and Medicine, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>81500063</GrantID><Agency>Natural Science for Youth Foundation, Beijing, China</Agency><Country></Country></Grant><Grant><GrantID>2018KJXX-034</GrantID><Agency>Innovative Talents Promotion Plan in Shaanxi Province, Xi'an, Shaanxi</Agency><Country></Country></Grant><Grant><GrantID>2016HXKF02</GrantID><Agency>Shaanxi Provincial Research Center for the Project of Prevention and Treatment of Respiratory Diseases, Xi'an, Shaanxi</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>09</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biochem Mol Toxicol</MedlineTA><NlmUniqueID>9717231</NlmUniqueID><ISSNLinking>1095-6670</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">IκBα</Keyword><Keyword MajorTopicYN="N">NF-κB</Keyword><Keyword MajorTopicYN="N">Nrf-2</Keyword><Keyword MajorTopicYN="N">TLR-4</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword><Keyword MajorTopicYN="N">lipopolysaccharide</Keyword><Keyword MajorTopicYN="N">pinitol</Keyword><Keyword MajorTopicYN="N">pneumonia</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>05</Month><Day>28</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>07</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>08</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>9</Month><Day>14</Day><Hour>15</Hour><Minute>50</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>9</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>9</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32926510</ArticleId><ArticleId IdType="doi">10.1002/jbt.22622</ArticleId></ArticleIdList><ReferenceList><Title>REFERENCES</Title><Reference><Citation>C. Walker, I. Rudan, L. Liu, H. Nair, E. Theodoratou, Z. A. Bhutta, K. L. O'Brien, H. Campbell, R. E. Black, Lancet 2013, 381, 1405.</Citation></Reference><Reference><Citation>J. K. Lee, J. Lee, Y. S. Park, C. H. Lee, J. J. Yim, C. G. Yoo, Y. W. Kim, S. K. Han, S. M. Lee, Korean J. Intern. Med. 2015, 30, 829.</Citation></Reference><Reference><Citation>A. Bjarnason, J. Westin, M. Lindh, L. M. Andersson, K. G. Kristinsson, A. Love, O. Baldursson, M. Gottfredsson, Open Forum Infect. Dis. 2018, 5, ofy010.</Citation></Reference><Reference><Citation>V. Sender, C. Stamme, Commun. Integr. Biol. 2014, 7, e29053.</Citation></Reference><Reference><Citation>L. Smeding, J. W. Kuiper, F. B. Plotz, M. C. Kneyber, A. J. Groeneveld, Respir. Res. 2013, 14, 92.</Citation></Reference><Reference><Citation>Y. Hu, J. Lou, Y. Y. Mao, T. W. Lai, L. Y. Liu, C. Zhu, C. Zhang, J. Liu, Y. Y. Li, F. Zhang, W. Li, S. M. Ying, Z. H. Chen, H. H. Shen, Autophagy 2016, 12, 2286.</Citation></Reference><Reference><Citation>A. D. Kandhare, Z. Liu, A. A. Mukherjee, S. L. Bodhankar, Curr. Mol. Pharmacol. 2019, 12, 122.</Citation></Reference><Reference><Citation>Y. L. Lee, W. Chen, L. Y. Chen, C. H. Chen, Y. C. Lin, S. J. Liang, C.-M. Shih, J. Crit. Care 2010, 25, e177.</Citation></Reference><Reference><Citation>Z. Tianzhu, Y. Shihai, D. Juan, Inflammation 2014, 37, 1976.</Citation></Reference><Reference><Citation>A. Strassburg, D. Droemann, G. van Zandbergen, H. Kothe, K. Dalhoff, Eur. Respir. J. 2004, 24, 772.</Citation></Reference><Reference><Citation>J. Kong, Z. Du, L. Dong, Neurotox. Res. 2020, 38, 96.</Citation></Reference><Reference><Citation>U. V. Shah, V. Karde, C. Ghoroi, J. Heng, Pediatrics 2016, 518, 138.</Citation></Reference><Reference><Citation>C. J. Russell, M. S. Shiroishi, E. Siantz, B. W. Wu, C. M. Patino, BMC Pulm. Med. 2016, 16, 40.</Citation></Reference><Reference><Citation>A. D. Kandhare, K. S. Raygude, P. Ghosh, T. P. Gosavi, S. L. Bodhankar, Int. J. Pharm. Biol. Arch. 2011, 2, 1024.</Citation></Reference><Reference><Citation>K. K. Nyati, K. Masuda, M. M. Zaman, P. K. Dubey, D. Millrine, J. P. Chalise, M. Higa, S. Li, D. M. Standley, K. Saito, H. Hanieh, T. Kishimoto, Nucleic Acids Res. 2017, 45, 2687.</Citation></Reference><Reference><Citation>Q. Yang, D. Wu, W. Mao, X. Liu, K. Bao, Q. Lin, F. Lu, C. Zou, C. Li, J. Evidence-Based Complementary Altern. Med. 2013, 2013, 203845.</Citation></Reference><Reference><Citation>E. S. Koh, S. Kim, M. Kim, Y. A. Hong, S. J. Shin, C. W. Park, Y. S. Chang, S. Chung, H. S. Kim, Int. J. Mol. Med. 2018, 41, 1826.</Citation></Reference><Reference><Citation>M. J. Kang, J. I. Kim, S. Y. Yoon, J. C. Kim, I. J. Cha, J. Med. Food 2006, 9, 182.</Citation></Reference><Reference><Citation>G. Sethi, K. S. Ahn, B. Sung, B. B. Aggarwal, Mol. Cancer Ther. 2008, 7, 1604.</Citation></Reference><Reference><Citation>J. S. Lee, C. M. Lee, Y. I. Jeong, I. D. Jung, B. H. Kim, E. Y. Seong, J. I. Kim, I. W. Choi, H. Y. Chung, Y. M. Park, FEBS Lett. 2007, 581, 57.</Citation></Reference><Reference><Citation>K. Zheng, Z. Zhao, N. Lin, Y. Wu, Y. Xu, W. Zhang, Med. Sci. Monit. 2017, 23, 1923.</Citation></Reference><Reference><Citation>E. Lee, Y. Lim, S. W. Kwon, O. Kwon, J. Nutr. Biochem. 2019, 68, 33.</Citation></Reference><Reference><Citation>A. D. Kandhare, S. L. Bodhankar, V. Mohan, P. A. Thakurdesai, Chem. Biol. Interact. 2015, 237, 151.</Citation></Reference><Reference><Citation>Y. Bei, T. Hua-Huy, S. Duong-Quy, V. H. Nguyen, W. Chen, C. Nicco, F. Batteux, A. T. Dinh-Xuan, Pulm. Pharmacol. Ther. 2013, 26, 635.</Citation></Reference><Reference><Citation>A. D. Kandhare, S. L. Bodhankar, V. Singh, V. Mohan, P. A. Thakurdesai, Biomed. Aging Pathol. 2013, 3, 23.</Citation></Reference><Reference><Citation>H. Kamble, A. D. Kandhare, S. L. Bodhankar, V. Mohan, P. A. Thakurdesai, Biomed. Aging Pathol. 2013, 3, 145.</Citation></Reference><Reference><Citation>A. D. Kandhare, K. S. Raygude, P. Ghosh, A. E. Ghule, S. L. Bodhankar, Fitoterapia 2012, 83, 650.</Citation></Reference><Reference><Citation>A. D. Kandhare, V. Shivakumar, A. Rajmane, P. Ghosh, S. L. Bodhankar, J. Nat. Med. 2014, 68, 586.</Citation></Reference><Reference><Citation>K. Liang, A. D. Kandhare, A. A. Mukherjee-Kandhare, S. L. Bodhankar, D. Xu, J Funct. Foods 2019, 55, 391.</Citation></Reference><Reference><Citation>Z. Zhou, A. D. Kandhare, A. A. Kandhare, S. L. Bodhankar, EXCLI J. 2019, 18, 723.</Citation></Reference><Reference><Citation>A. Haegens, P. Heeringa, R. J. van Suylen, C. Steele, Y. Aratani, R. J. O'Donoghue, S. E. Mutsaers, B. T. Mossman, E. F. Wouters, J. H. Vernooy, J. Immunol. 2009, 182, 7990.</Citation></Reference><Reference><Citation>A. A. Mukherjee, A. D. Kandhare, S. R. Rojatkar, S. L. Bodhankar, Biomed. Pharmacother. 2017, 94, 880.</Citation></Reference><Reference><Citation>C. J. Bae, J. W. Lee, S. B. Shim, S. W. Jee, S. H. Lee, J. M. Woo, C. K. Lee, D. Y. Hwang, Int. J. Mol. Med. 2011, 28, 171.</Citation></Reference><Reference><Citation>C. Zhao, Y. Wang, X. Yuan, G. Sun, B. Shen, F. Xu, G. Fan, M. Jin, X. Li, G. Liu, J. Dairy Res. 2019, 86, 171.</Citation></Reference><Reference><Citation>J. Chen, X. Liu, W. Du, R. Srivastava, J. Fu, M. Zheng, J. Zhou, E. McGrath, Glob. Pediatr. Health 2019, 6, 2333794X19840357.</Citation></Reference><Reference><Citation>A. Mukherjee, J. Zhang, A. D. Kandhare, S. L. Bodhankar, Lat. Am. J. Pharm. 2018, 37, 2502.</Citation></Reference><Reference><Citation>G. Zhang, A. D. Kandhare, A. A. Mukherjee, S. L. Bodhankar, H. Yin, Pharmacogn. Mag. 2019, 15, 43.</Citation></Reference><Reference><Citation>J. Wei, G. Chen, X. Shi, H. Zhou, M. Liu, Y. Chen, D. Feng, P. Zhang, L. Wu, X. Lv, Biochem. Biophys. Res. Commun. 2018, 500, 790.</Citation></Reference><Reference><Citation>A. D. Kandhare, A. Patil, A. Guru, A. Mukhrjee, S. Sarkar, A. Sengupta, H. M. Parmar, A. P. Muthal, P. Wangikar, S. L. Bodhankar, Pharmacologia 2015, 7, 114.</Citation></Reference><Reference><Citation>U. M. Aswar, A. D. Kandhare, V. Mohan, P. A. Thakurdesai, Phytother. Res. 2015, 29, 423.</Citation></Reference><Reference><Citation>F. Arnalich, E. Garcia-Palomero, J. López, M. Jiménez, R. Madero, J. Renart, J. J. Vázquez, C. Montiel, Infect. Immun. 2000, 68, 1942.</Citation></Reference><Reference><Citation>S. T. Devkar, A. D. Kandhare, A. A. Zanwar, S. D. Jagtap, S. S. Katyare, S. L. Bodhankar, M. V. Hegde, Pharm. Biol. 2016, 1.</Citation></Reference><Reference><Citation>A. D. Kandhare, M. V. Patil, S. L. Bodhankar, Ren. Fail. 2015, 37, 709.</Citation></Reference><Reference><Citation>N. Voskresenska, J. Voicehovska, S. Babikovs, L. Bergmane, M. Klibus, A. Lejnieks, Eur. Respir. J. 2017, 50, PA3934.</Citation></Reference><Reference><Citation>E. Moita, A. Gil-Izquierdo, C. Sousa, F. Ferreres, L. R. Silva, P. Valentão, R. Domínguez-Perles, N. Baenas, P. B. Andrade, PLOS One 2013, 8, e59131.</Citation></Reference><Reference><Citation>C. Li, D. Yang, X. Cao, F. Wang, H. Jiang, H. Guo, L. Du, Q. Guo, X. Yin, Biochem. Pharmacol. 2016, 113, 57.</Citation></Reference><Reference><Citation>R. A. Corrêa, A. N. Costa, F. Lundgren, L. Michelin, M. R. Figueiredo, M. Holanda, M. Gomes, P. Teixeira, R. Martins, R. Silva, R. A. Athanazio, R. Silva, M. C. Pereira, J. Bras. Pneumol. 2018, 44, 405.</Citation></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Fan, Yingying" sort="Fan, Yingying" uniqKey="Fan Y" first="Yingying" last="Fan">Yingying Fan</name></noRegion><name sortKey="Cao, Ke" sort="Cao, Ke" uniqKey="Cao K" first="Ke" last="Cao">Ke Cao</name><name sortKey="Feng, Zhihui" sort="Feng, Zhihui" uniqKey="Feng Z" first="Zhihui" last="Feng">Zhihui Feng</name><name sortKey="Liu, Jiankang" sort="Liu, Jiankang" uniqKey="Liu J" first="Jiankang" last="Liu">Jiankang Liu</name><name sortKey="Wang, Jian" sort="Wang, Jian" uniqKey="Wang J" first="Jian" last="Wang">Jian Wang</name><name sortKey="Xu, Hao" sort="Xu, Hao" uniqKey="Xu H" first="Hao" last="Xu">Hao Xu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Bois/explor/PlantImRecepV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000083 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000083 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Bois
|area= PlantImRecepV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:32926510
|texte= Pinitol attenuates LPS-induced pneumonia in experimental animals: Possible role via inhibition of the TLR-4 and NF-κB/IκBα signaling cascade pathway.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:32926510" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a PlantImRecepV1
| This area was generated with Dilib version V0.6.38. |  |