Acute lung injury induced by lipopolysaccharide is inhibited by wogonin in mice via reduction of Akt phosphorylation and RhoA activation
Objectives Neutrophil infiltration into the lung is the critical characteristic of acute lung injury (ALI), which is a clinical state with acute inflammatory syndrome. Up to now, there is no effective medicine for ALI. Wogonin has been shown to posses serval biological activities including anti‐infl...
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Veröffentlicht in: | Journal of pharmacy and pharmacology 2016-02, Vol.68 (2), p.257-263 |
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creator | Yeh, Yen-Cheng Yang, Ching-Ping Lee, Shiuan-Shinn Horng, Chi-Ting Chen, Hung-Yi Cho, Ta-Hsiung Yang, Ming-Ling Lee, Chien-Ying Li, Miao-Cing Kuan, Yu-Hsiang |
description | Objectives
Neutrophil infiltration into the lung is the critical characteristic of acute lung injury (ALI), which is a clinical state with acute inflammatory syndrome. Up to now, there is no effective medicine for ALI. Wogonin has been shown to posses serval biological activities including anti‐inflammation, anti‐oxidant and anti‐carcinoma.
Methods
Acute lung injury was induced by intratracheal injection of LPS, and wogonin at various concentrations was injected intraperitoneally 30 min prior to LPS. Contents of myeloperoxidase (MPO) and expression of chemokines and adhesion molecules were determined by commercially and ELISA assay kits, respectively. Akt phosphorylation and RhoA activation were measured by western blot and RhoA pull‐down activation assay, respectively.
Key finding
Neutrophil infiltration was reduced by wogonin in a concentration‐dependent manner in the LPS‐induced ALI mice model. LPS‐induced proinflammatory cytokines and adhesion molecules were inhibited by wogonin in bronchoalveolar lavage fluid (BALF) with LPS‐induced ALI. Furthermore, wogonin suppressed Akt phosphorylation and RhoA activation in lungs in LPS‐induced ALI. The similar parallel trend was observed as wogonin reduced LPS‐induced neutrophils infiltration, proinflammatory cytokines generation, adhesion molecules expression, Akt phosphorylation, and RhoA activation.
Summary
These results suggested that the effects of wogonin in LPS‐induced ALI were induced by inhibition of Akt phosphorylation and RhoA activation. |
doi_str_mv | 10.1111/jphp.12500 |
format | Article |
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Neutrophil infiltration into the lung is the critical characteristic of acute lung injury (ALI), which is a clinical state with acute inflammatory syndrome. Up to now, there is no effective medicine for ALI. Wogonin has been shown to posses serval biological activities including anti‐inflammation, anti‐oxidant and anti‐carcinoma.
Methods
Acute lung injury was induced by intratracheal injection of LPS, and wogonin at various concentrations was injected intraperitoneally 30 min prior to LPS. Contents of myeloperoxidase (MPO) and expression of chemokines and adhesion molecules were determined by commercially and ELISA assay kits, respectively. Akt phosphorylation and RhoA activation were measured by western blot and RhoA pull‐down activation assay, respectively.
Key finding
Neutrophil infiltration was reduced by wogonin in a concentration‐dependent manner in the LPS‐induced ALI mice model. LPS‐induced proinflammatory cytokines and adhesion molecules were inhibited by wogonin in bronchoalveolar lavage fluid (BALF) with LPS‐induced ALI. Furthermore, wogonin suppressed Akt phosphorylation and RhoA activation in lungs in LPS‐induced ALI. The similar parallel trend was observed as wogonin reduced LPS‐induced neutrophils infiltration, proinflammatory cytokines generation, adhesion molecules expression, Akt phosphorylation, and RhoA activation.
Summary
These results suggested that the effects of wogonin in LPS‐induced ALI were induced by inhibition of Akt phosphorylation and RhoA activation.</description><identifier>ISSN: 0022-3573</identifier><identifier>EISSN: 2042-7158</identifier><identifier>DOI: 10.1111/jphp.12500</identifier><identifier>PMID: 26749510</identifier><identifier>CODEN: JPPMAB</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>acute lung injury ; Acute Lung Injury - chemically induced ; Acute Lung Injury - immunology ; Acute Lung Injury - metabolism ; Acute Lung Injury - prevention & control ; adhesion molecules ; Akt ; Animals ; Cytokines ; Drugs, Chinese Herbal - administration & dosage ; Drugs, Chinese Herbal - therapeutic use ; Flavanones - administration & dosage ; Flavanones - therapeutic use ; Intercellular Adhesion Molecule-1 - metabolism ; Lipopolysaccharides - toxicity ; Male ; Mice, Inbred ICR ; Neutrophils ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; rho GTP-Binding Proteins - metabolism ; RhoA ; Rodents ; Scutellaria - chemistry ; Vascular Cell Adhesion Molecule-1 - metabolism ; wogonin</subject><ispartof>Journal of pharmacy and pharmacology, 2016-02, Vol.68 (2), p.257-263</ispartof><rights>2016 Royal Pharmaceutical Society</rights><rights>2016 Royal Pharmaceutical Society.</rights><rights>Copyright © 2016 Royal Pharmaceutical Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4980-c0be1f43755bdcd808220609f1b42789b7487ca9fbffbc9490311fbc7b8536483</citedby><cites>FETCH-LOGICAL-c4980-c0be1f43755bdcd808220609f1b42789b7487ca9fbffbc9490311fbc7b8536483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fjphp.12500$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fjphp.12500$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26749510$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yeh, Yen-Cheng</creatorcontrib><creatorcontrib>Yang, Ching-Ping</creatorcontrib><creatorcontrib>Lee, Shiuan-Shinn</creatorcontrib><creatorcontrib>Horng, Chi-Ting</creatorcontrib><creatorcontrib>Chen, Hung-Yi</creatorcontrib><creatorcontrib>Cho, Ta-Hsiung</creatorcontrib><creatorcontrib>Yang, Ming-Ling</creatorcontrib><creatorcontrib>Lee, Chien-Ying</creatorcontrib><creatorcontrib>Li, Miao-Cing</creatorcontrib><creatorcontrib>Kuan, Yu-Hsiang</creatorcontrib><title>Acute lung injury induced by lipopolysaccharide is inhibited by wogonin in mice via reduction of Akt phosphorylation and RhoA activation</title><title>Journal of pharmacy and pharmacology</title><addtitle>J Pharm Pharmacol</addtitle><description>Objectives
Neutrophil infiltration into the lung is the critical characteristic of acute lung injury (ALI), which is a clinical state with acute inflammatory syndrome. Up to now, there is no effective medicine for ALI. Wogonin has been shown to posses serval biological activities including anti‐inflammation, anti‐oxidant and anti‐carcinoma.
Methods
Acute lung injury was induced by intratracheal injection of LPS, and wogonin at various concentrations was injected intraperitoneally 30 min prior to LPS. Contents of myeloperoxidase (MPO) and expression of chemokines and adhesion molecules were determined by commercially and ELISA assay kits, respectively. Akt phosphorylation and RhoA activation were measured by western blot and RhoA pull‐down activation assay, respectively.
Key finding
Neutrophil infiltration was reduced by wogonin in a concentration‐dependent manner in the LPS‐induced ALI mice model. LPS‐induced proinflammatory cytokines and adhesion molecules were inhibited by wogonin in bronchoalveolar lavage fluid (BALF) with LPS‐induced ALI. Furthermore, wogonin suppressed Akt phosphorylation and RhoA activation in lungs in LPS‐induced ALI. The similar parallel trend was observed as wogonin reduced LPS‐induced neutrophils infiltration, proinflammatory cytokines generation, adhesion molecules expression, Akt phosphorylation, and RhoA activation.
Summary
These results suggested that the effects of wogonin in LPS‐induced ALI were induced by inhibition of Akt phosphorylation and RhoA activation.</description><subject>acute lung injury</subject><subject>Acute Lung Injury - chemically induced</subject><subject>Acute Lung Injury - immunology</subject><subject>Acute Lung Injury - metabolism</subject><subject>Acute Lung Injury - prevention & control</subject><subject>adhesion molecules</subject><subject>Akt</subject><subject>Animals</subject><subject>Cytokines</subject><subject>Drugs, Chinese Herbal - administration & dosage</subject><subject>Drugs, Chinese Herbal - therapeutic use</subject><subject>Flavanones - administration & dosage</subject><subject>Flavanones - therapeutic use</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Male</subject><subject>Mice, Inbred ICR</subject><subject>Neutrophils</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>rho GTP-Binding Proteins - metabolism</subject><subject>RhoA</subject><subject>Rodents</subject><subject>Scutellaria - chemistry</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><subject>wogonin</subject><issn>0022-3573</issn><issn>2042-7158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqN0VFr1TAUB_AgirtOX_wAEvBFhM6TtEnax8vQXWXqEJ3gS0jSdM1db1OTdrPfwI9tdrvtwQcxEBIOv_OH5CD0nMARSevNdmiHI0IZwAO0olDQTBBWPkQrAEqznIn8AD2JcQsAgnP-GB1QLoqKEVih32szjRZ3U3-BXb-dwpyOejK2xnrGnRv84Ls5KmNaFVxtsYsJtE67cSHX_sL3rk9FvHPG4iuncLApYXS-x77B68sRD62PaYe5U_uy6mv8pfVrrBK72teeokeN6qJ9dnseom_v3n493mSnn0_eH69PM1NUJWQGtCVNkQvGdG3qEkpKgUPVEF1QUVZaFKUwqmp002hTFRXkhKSb0CXLeVHmh-jVkjsE_3OycZQ7F43tOtVbP0VJRAkMGCf8PyhnFeEVsERf_kW3fgp9esheUU7ynCb1elEm-BiDbeQQ3E6FWRKQN6OUN6OU-1Em_OI2ctI7W9_Tu9klQBZw7To7_yNKfjjbnN2FZkuPi6P9dd-jwqXkIn2q_P7pRJ4LoD825x8ly_8A7Me49A</recordid><startdate>201602</startdate><enddate>201602</enddate><creator>Yeh, Yen-Cheng</creator><creator>Yang, Ching-Ping</creator><creator>Lee, Shiuan-Shinn</creator><creator>Horng, Chi-Ting</creator><creator>Chen, Hung-Yi</creator><creator>Cho, Ta-Hsiung</creator><creator>Yang, Ming-Ling</creator><creator>Lee, Chien-Ying</creator><creator>Li, Miao-Cing</creator><creator>Kuan, Yu-Hsiang</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>7X8</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>201602</creationdate><title>Acute lung injury induced by lipopolysaccharide is inhibited by wogonin in mice via reduction of Akt phosphorylation and RhoA activation</title><author>Yeh, Yen-Cheng ; Yang, Ching-Ping ; Lee, Shiuan-Shinn ; Horng, Chi-Ting ; Chen, Hung-Yi ; Cho, Ta-Hsiung ; Yang, Ming-Ling ; Lee, Chien-Ying ; Li, Miao-Cing ; Kuan, Yu-Hsiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4980-c0be1f43755bdcd808220609f1b42789b7487ca9fbffbc9490311fbc7b8536483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>acute lung injury</topic><topic>Acute Lung Injury - chemically induced</topic><topic>Acute Lung Injury - immunology</topic><topic>Acute Lung Injury - metabolism</topic><topic>Acute Lung Injury - prevention & control</topic><topic>adhesion molecules</topic><topic>Akt</topic><topic>Animals</topic><topic>Cytokines</topic><topic>Drugs, Chinese Herbal - administration & dosage</topic><topic>Drugs, Chinese Herbal - therapeutic use</topic><topic>Flavanones - administration & dosage</topic><topic>Flavanones - therapeutic use</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Male</topic><topic>Mice, Inbred ICR</topic><topic>Neutrophils</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>rho GTP-Binding Proteins - metabolism</topic><topic>RhoA</topic><topic>Rodents</topic><topic>Scutellaria - chemistry</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><topic>wogonin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yeh, Yen-Cheng</creatorcontrib><creatorcontrib>Yang, Ching-Ping</creatorcontrib><creatorcontrib>Lee, Shiuan-Shinn</creatorcontrib><creatorcontrib>Horng, Chi-Ting</creatorcontrib><creatorcontrib>Chen, Hung-Yi</creatorcontrib><creatorcontrib>Cho, Ta-Hsiung</creatorcontrib><creatorcontrib>Yang, Ming-Ling</creatorcontrib><creatorcontrib>Lee, Chien-Ying</creatorcontrib><creatorcontrib>Li, Miao-Cing</creatorcontrib><creatorcontrib>Kuan, Yu-Hsiang</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Journal of pharmacy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yeh, Yen-Cheng</au><au>Yang, Ching-Ping</au><au>Lee, Shiuan-Shinn</au><au>Horng, Chi-Ting</au><au>Chen, Hung-Yi</au><au>Cho, Ta-Hsiung</au><au>Yang, Ming-Ling</au><au>Lee, Chien-Ying</au><au>Li, Miao-Cing</au><au>Kuan, Yu-Hsiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute lung injury induced by lipopolysaccharide is inhibited by wogonin in mice via reduction of Akt phosphorylation and RhoA activation</atitle><jtitle>Journal of pharmacy and pharmacology</jtitle><addtitle>J Pharm Pharmacol</addtitle><date>2016-02</date><risdate>2016</risdate><volume>68</volume><issue>2</issue><spage>257</spage><epage>263</epage><pages>257-263</pages><issn>0022-3573</issn><eissn>2042-7158</eissn><coden>JPPMAB</coden><abstract>Objectives
Neutrophil infiltration into the lung is the critical characteristic of acute lung injury (ALI), which is a clinical state with acute inflammatory syndrome. Up to now, there is no effective medicine for ALI. Wogonin has been shown to posses serval biological activities including anti‐inflammation, anti‐oxidant and anti‐carcinoma.
Methods
Acute lung injury was induced by intratracheal injection of LPS, and wogonin at various concentrations was injected intraperitoneally 30 min prior to LPS. Contents of myeloperoxidase (MPO) and expression of chemokines and adhesion molecules were determined by commercially and ELISA assay kits, respectively. Akt phosphorylation and RhoA activation were measured by western blot and RhoA pull‐down activation assay, respectively.
Key finding
Neutrophil infiltration was reduced by wogonin in a concentration‐dependent manner in the LPS‐induced ALI mice model. LPS‐induced proinflammatory cytokines and adhesion molecules were inhibited by wogonin in bronchoalveolar lavage fluid (BALF) with LPS‐induced ALI. Furthermore, wogonin suppressed Akt phosphorylation and RhoA activation in lungs in LPS‐induced ALI. The similar parallel trend was observed as wogonin reduced LPS‐induced neutrophils infiltration, proinflammatory cytokines generation, adhesion molecules expression, Akt phosphorylation, and RhoA activation.
Summary
These results suggested that the effects of wogonin in LPS‐induced ALI were induced by inhibition of Akt phosphorylation and RhoA activation.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>26749510</pmid><doi>10.1111/jphp.12500</doi><tpages>7</tpages></addata></record> |
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source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); Wiley Online Library All Journals |
subjects | acute lung injury Acute Lung Injury - chemically induced Acute Lung Injury - immunology Acute Lung Injury - metabolism Acute Lung Injury - prevention & control adhesion molecules Akt Animals Cytokines Drugs, Chinese Herbal - administration & dosage Drugs, Chinese Herbal - therapeutic use Flavanones - administration & dosage Flavanones - therapeutic use Intercellular Adhesion Molecule-1 - metabolism Lipopolysaccharides - toxicity Male Mice, Inbred ICR Neutrophils Phosphorylation Proto-Oncogene Proteins c-akt - metabolism rho GTP-Binding Proteins - metabolism RhoA Rodents Scutellaria - chemistry Vascular Cell Adhesion Molecule-1 - metabolism wogonin |
title | Acute lung injury induced by lipopolysaccharide is inhibited by wogonin in mice via reduction of Akt phosphorylation and RhoA activation |
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