Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages
Thunbergia alata (Acanthaceae) has been used traditionally to treat various inflammatory diseases such as fever, cough and diarrhea in East African countries including Uganda and Kenya. However, systemic studies elucidating the anti-inflammatory effects and precise mechanisms of action of T. alata h...
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| Veröffentlicht in: | International journal of molecular medicine 2016-11, Vol.38 (5), p.1596-1604 |
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| creator | Cho, Young-Chang Kim, Ye Rang Kim, Ba Reum Bach, Tran The Cho, Sayeon |
| description | Thunbergia alata (Acanthaceae) has been used traditionally to treat various inflammatory diseases such as fever, cough and diarrhea in East African countries including Uganda and Kenya. However, systemic studies elucidating the anti-inflammatory effects and precise mechanisms of action of T. alata have not been conducted, to the best of our knowledge. To address these concerns, we explored the anti-inflammatory effects of a methanol extract of T. alata (MTA) in macrophages. Non-cytotoxic concentrations of MTA (≤300 μg/ml) inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages by transcriptional regulation of inducible NO synthase in a dose-dependent manner. The expression of cyclooxygenase-2, the enzyme responsible for the production of prostaglandin E2, was unchanged by MTA at the mRNA and protein levels. MTA treatment inhibited interleukin (IL)-6 inflammatory cytokines, including IL-6 and IL-1β. Tumor necrosis factor-α production and mRNA expression were not regulated by MTA treatment. The decreased production of inflammatory mediators by MTA was followed by the reduced phosphorylation of extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3). MTA treatment had no effect on activity of other mitogen-activated protein kinases (MAPKs), p38, c-Jun N-terminal kinase (JNK), and nuclear factor-κB (NF-κB). These results indicate that MTA selectively inhibits the excessive production of inflammatory mediators in LPS-stimulated murine macrophages by reducing the activity of ERK and STAT3, suggesting that MTA plays an important inhibitory role in the modulation of severe inflammation. |
| doi_str_mv | 10.3892/ijmm.2016.2746 |
| format | Article |
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However, systemic studies elucidating the anti-inflammatory effects and precise mechanisms of action of T. alata have not been conducted, to the best of our knowledge. To address these concerns, we explored the anti-inflammatory effects of a methanol extract of T. alata (MTA) in macrophages. Non-cytotoxic concentrations of MTA (≤300 μg/ml) inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages by transcriptional regulation of inducible NO synthase in a dose-dependent manner. The expression of cyclooxygenase-2, the enzyme responsible for the production of prostaglandin E2, was unchanged by MTA at the mRNA and protein levels. MTA treatment inhibited interleukin (IL)-6 inflammatory cytokines, including IL-6 and IL-1β. Tumor necrosis factor-α production and mRNA expression were not regulated by MTA treatment. The decreased production of inflammatory mediators by MTA was followed by the reduced phosphorylation of extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3). MTA treatment had no effect on activity of other mitogen-activated protein kinases (MAPKs), p38, c-Jun N-terminal kinase (JNK), and nuclear factor-κB (NF-κB). These results indicate that MTA selectively inhibits the excessive production of inflammatory mediators in LPS-stimulated murine macrophages by reducing the activity of ERK and STAT3, suggesting that MTA plays an important inhibitory role in the modulation of severe inflammation.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2016.2746</identifier><identifier>PMID: 27666485</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Acanthaceae - chemistry ; Animals ; Blotting, Western ; Care and treatment ; Cell Line ; Dose-Response Relationship, Drug ; Enzyme Activation - drug effects ; extracellular signal-regulated kinase ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Gene Expression - drug effects ; Genetic aspects ; Health aspects ; Immune system ; Inflammation ; Inflammation - genetics ; Inflammation - metabolism ; Inflammation - prevention & control ; Inflammatory diseases ; interleukin 6 ; Interleukin-1beta - genetics ; Interleukin-1beta - metabolism ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Kinases ; Lipopolysaccharides - pharmacology ; Macrophages - drug effects ; Macrophages - metabolism ; Materia medica, Vegetable ; Medical research ; Methanol - chemistry ; Mice ; nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Phosphorylation ; Phosphorylation - drug effects ; Phytochemicals ; Plant extracts ; Plant Extracts - pharmacology ; Production increases ; Prostaglandin-Endoperoxide Synthases - genetics ; Prostaglandin-Endoperoxide Synthases - metabolism ; Regulation ; Reverse Transcriptase Polymerase Chain Reaction ; signal transducer and activator of transcription 3 ; Signal transduction ; STAT3 Transcription Factor - metabolism ; Studies ; Thunbergia alata ; Transcription factors ; Tumor necrosis factor-TNF ; tumor necrosis factor-α</subject><ispartof>International journal of molecular medicine, 2016-11, Vol.38 (5), p.1596-1604</ispartof><rights>Copyright © 2016, Spandidos Publications</rights><rights>COPYRIGHT 2016 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-52e692e86ad7c33ece0c9a670edcbfcfed9f81b7ac4840d622ca16fd174c41673</citedby><cites>FETCH-LOGICAL-c463t-52e692e86ad7c33ece0c9a670edcbfcfed9f81b7ac4840d622ca16fd174c41673</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,5571,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27666485$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cho, Young-Chang</creatorcontrib><creatorcontrib>Kim, Ye Rang</creatorcontrib><creatorcontrib>Kim, Ba Reum</creatorcontrib><creatorcontrib>Bach, Tran The</creatorcontrib><creatorcontrib>Cho, Sayeon</creatorcontrib><title>Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Thunbergia alata (Acanthaceae) has been used traditionally to treat various inflammatory diseases such as fever, cough and diarrhea in East African countries including Uganda and Kenya. However, systemic studies elucidating the anti-inflammatory effects and precise mechanisms of action of T. alata have not been conducted, to the best of our knowledge. To address these concerns, we explored the anti-inflammatory effects of a methanol extract of T. alata (MTA) in macrophages. Non-cytotoxic concentrations of MTA (≤300 μg/ml) inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages by transcriptional regulation of inducible NO synthase in a dose-dependent manner. The expression of cyclooxygenase-2, the enzyme responsible for the production of prostaglandin E2, was unchanged by MTA at the mRNA and protein levels. MTA treatment inhibited interleukin (IL)-6 inflammatory cytokines, including IL-6 and IL-1β. Tumor necrosis factor-α production and mRNA expression were not regulated by MTA treatment. The decreased production of inflammatory mediators by MTA was followed by the reduced phosphorylation of extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3). MTA treatment had no effect on activity of other mitogen-activated protein kinases (MAPKs), p38, c-Jun N-terminal kinase (JNK), and nuclear factor-κB (NF-κB). These results indicate that MTA selectively inhibits the excessive production of inflammatory mediators in LPS-stimulated murine macrophages by reducing the activity of ERK and STAT3, suggesting that MTA plays an important inhibitory role in the modulation of severe inflammation.</description><subject>Acanthaceae - chemistry</subject><subject>Animals</subject><subject>Blotting, Western</subject><subject>Care and treatment</subject><subject>Cell Line</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Activation - drug effects</subject><subject>extracellular signal-regulated kinase</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Gene Expression - drug effects</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - prevention & control</subject><subject>Inflammatory diseases</subject><subject>interleukin 6</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Kinases</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Materia medica, Vegetable</subject><subject>Medical research</subject><subject>Methanol - chemistry</subject><subject>Mice</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Phytochemicals</subject><subject>Plant extracts</subject><subject>Plant Extracts - pharmacology</subject><subject>Production increases</subject><subject>Prostaglandin-Endoperoxide Synthases - genetics</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Regulation</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>signal transducer and activator of transcription 3</subject><subject>Signal transduction</subject><subject>STAT3 Transcription Factor - metabolism</subject><subject>Studies</subject><subject>Thunbergia alata</subject><subject>Transcription factors</subject><subject>Tumor necrosis factor-TNF</subject><subject>tumor necrosis factor-α</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkU1r3DAQhk1paNK01x6LoJdevNGXJeu4hKQNDRSSLfQmxpK81rK2XEkO5N9XJml6CTrMoHnm1YzeqvpE8Ia1il74wzhuKCZiQyUXb6ozIhWpKee_35acYFkz2YjT6n1KB4xpw1X7rjqlUgjB2-as8rthmToX9x4QHCED8tPgO59TSfojjCPkEB9RdGkOU3IJ5SGGZT-U6AoCJvsHyD5MKPTo6u4Hgsmi-912x0oVjWBimAfYu_ShOunhmNzH53he_bq-2l1-r29_fru53N7WhguW64Y6oahrBVhpGHPGYaNASOys6XrTO6v6lnQSDG85toJSA0T0lkhuOBGSnVdfnnTnGP4sLmV9CEucypOaKEYZbRRp_1N7ODpdVg05ghl9MnrLJSMCK7JqbV6hyrFu9CZMrvfl_rWGsnZK0fV6jn6E-KgJ1qthejVMr4bp1bDS8Pl52qUbnX3B_zlUgK9PQJrLz3ob0guzStWsrXFTk0YJ9hdlyp8T</recordid><startdate>20161101</startdate><enddate>20161101</enddate><creator>Cho, Young-Chang</creator><creator>Kim, Ye Rang</creator><creator>Kim, Ba Reum</creator><creator>Bach, Tran The</creator><creator>Cho, Sayeon</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20161101</creationdate><title>Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages</title><author>Cho, Young-Chang ; Kim, Ye Rang ; Kim, Ba Reum ; Bach, Tran The ; Cho, Sayeon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-52e692e86ad7c33ece0c9a670edcbfcfed9f81b7ac4840d622ca16fd174c41673</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acanthaceae - chemistry</topic><topic>Animals</topic><topic>Blotting, Western</topic><topic>Care and treatment</topic><topic>Cell Line</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Activation - drug effects</topic><topic>extracellular signal-regulated kinase</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Gene Expression - drug effects</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Inflammation - genetics</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - prevention & control</topic><topic>Inflammatory diseases</topic><topic>interleukin 6</topic><topic>Interleukin-1beta - genetics</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Kinases</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Materia medica, Vegetable</topic><topic>Medical research</topic><topic>Methanol - chemistry</topic><topic>Mice</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Phytochemicals</topic><topic>Plant extracts</topic><topic>Plant Extracts - pharmacology</topic><topic>Production increases</topic><topic>Prostaglandin-Endoperoxide Synthases - genetics</topic><topic>Prostaglandin-Endoperoxide Synthases - metabolism</topic><topic>Regulation</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>signal transducer and activator of transcription 3</topic><topic>Signal transduction</topic><topic>STAT3 Transcription Factor - metabolism</topic><topic>Studies</topic><topic>Thunbergia alata</topic><topic>Transcription factors</topic><topic>Tumor necrosis factor-TNF</topic><topic>tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cho, Young-Chang</creatorcontrib><creatorcontrib>Kim, Ye Rang</creatorcontrib><creatorcontrib>Kim, Ba Reum</creatorcontrib><creatorcontrib>Bach, Tran The</creatorcontrib><creatorcontrib>Cho, Sayeon</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>International journal of molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cho, Young-Chang</au><au>Kim, Ye Rang</au><au>Kim, Ba Reum</au><au>Bach, Tran The</au><au>Cho, Sayeon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages</atitle><jtitle>International journal of molecular medicine</jtitle><addtitle>Int J Mol Med</addtitle><date>2016-11-01</date><risdate>2016</risdate><volume>38</volume><issue>5</issue><spage>1596</spage><epage>1604</epage><pages>1596-1604</pages><issn>1107-3756</issn><eissn>1791-244X</eissn><abstract>Thunbergia alata (Acanthaceae) has been used traditionally to treat various inflammatory diseases such as fever, cough and diarrhea in East African countries including Uganda and Kenya. However, systemic studies elucidating the anti-inflammatory effects and precise mechanisms of action of T. alata have not been conducted, to the best of our knowledge. To address these concerns, we explored the anti-inflammatory effects of a methanol extract of T. alata (MTA) in macrophages. Non-cytotoxic concentrations of MTA (≤300 μg/ml) inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages by transcriptional regulation of inducible NO synthase in a dose-dependent manner. The expression of cyclooxygenase-2, the enzyme responsible for the production of prostaglandin E2, was unchanged by MTA at the mRNA and protein levels. MTA treatment inhibited interleukin (IL)-6 inflammatory cytokines, including IL-6 and IL-1β. Tumor necrosis factor-α production and mRNA expression were not regulated by MTA treatment. The decreased production of inflammatory mediators by MTA was followed by the reduced phosphorylation of extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription 3 (STAT3). MTA treatment had no effect on activity of other mitogen-activated protein kinases (MAPKs), p38, c-Jun N-terminal kinase (JNK), and nuclear factor-κB (NF-κB). These results indicate that MTA selectively inhibits the excessive production of inflammatory mediators in LPS-stimulated murine macrophages by reducing the activity of ERK and STAT3, suggesting that MTA plays an important inhibitory role in the modulation of severe inflammation.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>27666485</pmid><doi>10.3892/ijmm.2016.2746</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of molecular medicine, 2016-11, Vol.38 (5), p.1596-1604 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acanthaceae - chemistry Animals Blotting, Western Care and treatment Cell Line Dose-Response Relationship, Drug Enzyme Activation - drug effects extracellular signal-regulated kinase Extracellular Signal-Regulated MAP Kinases - metabolism Gene Expression - drug effects Genetic aspects Health aspects Immune system Inflammation Inflammation - genetics Inflammation - metabolism Inflammation - prevention & control Inflammatory diseases interleukin 6 Interleukin-1beta - genetics Interleukin-1beta - metabolism Interleukin-6 - genetics Interleukin-6 - metabolism Kinases Lipopolysaccharides - pharmacology Macrophages - drug effects Macrophages - metabolism Materia medica, Vegetable Medical research Methanol - chemistry Mice nitric oxide Nitric Oxide - metabolism Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Phosphorylation Phosphorylation - drug effects Phytochemicals Plant extracts Plant Extracts - pharmacology Production increases Prostaglandin-Endoperoxide Synthases - genetics Prostaglandin-Endoperoxide Synthases - metabolism Regulation Reverse Transcriptase Polymerase Chain Reaction signal transducer and activator of transcription 3 Signal transduction STAT3 Transcription Factor - metabolism Studies Thunbergia alata Transcription factors Tumor necrosis factor-TNF tumor necrosis factor-α |
| title | Thunbergia alata inhibits inflammatory responses through the inactivation of ERK and STAT3 in macrophages |
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