Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect
ACTG-toxin H (AH) originates from Alternaria sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression a...
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| Veröffentlicht in: | Molecular and cellular biochemistry 2013-02, Vol.374 (1-2), p.29-36 |
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| container_title | Molecular and cellular biochemistry |
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| creator | Yang, Xinying Zhang, Guojian Tang, Xuelian Jiao, Jieying Kim, Sung Yeon Lee, Joo Young Zhu, Tianjiao Li, Dehai Yun, Yong Gab Gu, Qianqun Park, Hyun |
| description | ACTG-toxin H (AH) originates from
Alternaria
sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-κB (NFκB) DNA-binding activity. Using transfection assay and measurement of an NFκB-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NFκB transcription activity in 293T cells. AH significantly blocked LPS-induced NFκB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFκB signaling pathway. |
| doi_str_mv | 10.1007/s11010-012-1502-9 |
| format | Article |
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Alternaria
sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-κB (NFκB) DNA-binding activity. Using transfection assay and measurement of an NFκB-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NFκB transcription activity in 293T cells. AH significantly blocked LPS-induced NFκB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFκB signaling pathway.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-012-1502-9</identifier><identifier>PMID: 23139166</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>AKT protein ; Alternaria ; Alternaria - metabolism ; Animals ; Anti-Inflammatory Agents - pharmacology ; Biochemistry ; Biomedical and Life Sciences ; Cardiology ; Cell Line ; Cell Survival ; COX-2 inhibitors ; Cyclooxygenase 2 - metabolism ; DNA ; DNA-Binding Proteins - metabolism ; Enzyme Activation - drug effects ; Enzymes ; Genetic research ; HEK293 Cells ; Humans ; Infection ; Inflammation - immunology ; Interleukin-1beta - metabolism ; Interleukin-6 - metabolism ; Life Sciences ; Lipopolysaccharides ; Macrophages - metabolism ; Medical Biochemistry ; Mice ; Mitogens ; Mycotoxins - pharmacology ; NF-kappa B - metabolism ; Nitric oxide ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase Type II - metabolism ; Oncology ; p38 Mitogen-Activated Protein Kinases - metabolism ; Proto-Oncogene Proteins c-akt - metabolism ; Signal Transduction ; T cells ; Toll-Like Receptor 4 - genetics ; Toll-Like Receptor 4 - metabolism</subject><ispartof>Molecular and cellular biochemistry, 2013-02, Vol.374 (1-2), p.29-36</ispartof><rights>Springer Science+Business Media New York 2012</rights><rights>COPYRIGHT 2013 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-dad50178c1b575615b2d089a3127d5b19c34f1c0e9e89a9d1022023a03d46d323</citedby><cites>FETCH-LOGICAL-c444t-dad50178c1b575615b2d089a3127d5b19c34f1c0e9e89a9d1022023a03d46d323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-012-1502-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-012-1502-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23139166$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Xinying</creatorcontrib><creatorcontrib>Zhang, Guojian</creatorcontrib><creatorcontrib>Tang, Xuelian</creatorcontrib><creatorcontrib>Jiao, Jieying</creatorcontrib><creatorcontrib>Kim, Sung Yeon</creatorcontrib><creatorcontrib>Lee, Joo Young</creatorcontrib><creatorcontrib>Zhu, Tianjiao</creatorcontrib><creatorcontrib>Li, Dehai</creatorcontrib><creatorcontrib>Yun, Yong Gab</creatorcontrib><creatorcontrib>Gu, Qianqun</creatorcontrib><creatorcontrib>Park, Hyun</creatorcontrib><title>Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>ACTG-toxin H (AH) originates from
Alternaria
sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-κB (NFκB) DNA-binding activity. Using transfection assay and measurement of an NFκB-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NFκB transcription activity in 293T cells. AH significantly blocked LPS-induced NFκB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFκB signaling pathway.</description><subject>AKT protein</subject><subject>Alternaria</subject><subject>Alternaria - metabolism</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cardiology</subject><subject>Cell Line</subject><subject>Cell Survival</subject><subject>COX-2 inhibitors</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>DNA</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Enzyme Activation - drug effects</subject><subject>Enzymes</subject><subject>Genetic research</subject><subject>HEK293 Cells</subject><subject>Humans</subject><subject>Infection</subject><subject>Inflammation - immunology</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukin-6 - metabolism</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides</subject><subject>Macrophages - metabolism</subject><subject>Medical Biochemistry</subject><subject>Mice</subject><subject>Mitogens</subject><subject>Mycotoxins - pharmacology</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Oncology</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal Transduction</subject><subject>T cells</subject><subject>Toll-Like Receptor 4 - genetics</subject><subject>Toll-Like Receptor 4 - metabolism</subject><issn>0300-8177</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9uEzEQxi0EoqHwAFzQSly4uJ2x9098DBG0SJW4hLPl2LPBxbsO9qZtXo2H4JlwtAUJCSEfPJr5fZ9G8zH2GuECAbrLjAgIHFBwbEBw9YQtsOkkrxWqp2wBEoAvsevO2Iucb6HAgPicnQmJUmHbLtj9JobAg_9GVSJL-ymmqr4cDzaQSVVvbGnwnz_eV9nvRhP8uKv2Zvp6b46Vz5Uf72K4I1eKarXeXPEpPpTymg_kvJnKwIyT537sgxkGU7yOFfU92ekle9abkOnV43_Ovnz8sFlf85vPV5_Wqxtu67qeuDOuAeyWFrdN17TYbIWDpTISReeaLSor6x4tkKLSVQ5BCBDSgHR166SQ5-zd7LtP8fuB8qQHny2FYEaKh6yxbusGlAQs6NsZ3ZlAuuwcp2TsCdcrKdtyRlCqUBf_oMpzNHgbR-p96f8lwFlgU8w5Ua_3yQ8mHTWCPsWo5xh1iVGfYtQnzZvHrQ_bcso_it-5FUDMQC6jcUdJ38ZDKgHl_7j-ArkYpo0</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>Yang, Xinying</creator><creator>Zhang, Guojian</creator><creator>Tang, Xuelian</creator><creator>Jiao, Jieying</creator><creator>Kim, Sung Yeon</creator><creator>Lee, Joo Young</creator><creator>Zhu, Tianjiao</creator><creator>Li, Dehai</creator><creator>Yun, Yong Gab</creator><creator>Gu, Qianqun</creator><creator>Park, Hyun</creator><general>Springer US</general><general>Springer</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>7T5</scope><scope>H94</scope></search><sort><creationdate>20130201</creationdate><title>Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect</title><author>Yang, Xinying ; Zhang, Guojian ; Tang, Xuelian ; Jiao, Jieying ; Kim, Sung Yeon ; Lee, Joo Young ; Zhu, Tianjiao ; Li, Dehai ; Yun, Yong Gab ; Gu, Qianqun ; Park, Hyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-dad50178c1b575615b2d089a3127d5b19c34f1c0e9e89a9d1022023a03d46d323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>AKT protein</topic><topic>Alternaria</topic><topic>Alternaria - metabolism</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cardiology</topic><topic>Cell Line</topic><topic>Cell Survival</topic><topic>COX-2 inhibitors</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>DNA</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Enzyme Activation - drug effects</topic><topic>Enzymes</topic><topic>Genetic research</topic><topic>HEK293 Cells</topic><topic>Humans</topic><topic>Infection</topic><topic>Inflammation - immunology</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukin-6 - metabolism</topic><topic>Life Sciences</topic><topic>Lipopolysaccharides</topic><topic>Macrophages - metabolism</topic><topic>Medical Biochemistry</topic><topic>Mice</topic><topic>Mitogens</topic><topic>Mycotoxins - pharmacology</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Oncology</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal Transduction</topic><topic>T cells</topic><topic>Toll-Like Receptor 4 - genetics</topic><topic>Toll-Like Receptor 4 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Xinying</creatorcontrib><creatorcontrib>Zhang, Guojian</creatorcontrib><creatorcontrib>Tang, Xuelian</creatorcontrib><creatorcontrib>Jiao, Jieying</creatorcontrib><creatorcontrib>Kim, Sung Yeon</creatorcontrib><creatorcontrib>Lee, Joo Young</creatorcontrib><creatorcontrib>Zhu, Tianjiao</creatorcontrib><creatorcontrib>Li, Dehai</creatorcontrib><creatorcontrib>Yun, Yong Gab</creatorcontrib><creatorcontrib>Gu, Qianqun</creatorcontrib><creatorcontrib>Park, Hyun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Molecular and cellular biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Xinying</au><au>Zhang, Guojian</au><au>Tang, Xuelian</au><au>Jiao, Jieying</au><au>Kim, Sung Yeon</au><au>Lee, Joo Young</au><au>Zhu, Tianjiao</au><au>Li, Dehai</au><au>Yun, Yong Gab</au><au>Gu, Qianqun</au><au>Park, Hyun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect</atitle><jtitle>Molecular and cellular biochemistry</jtitle><stitle>Mol Cell Biochem</stitle><addtitle>Mol Cell Biochem</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>374</volume><issue>1-2</issue><spage>29</spage><epage>36</epage><pages>29-36</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>ACTG-toxin H (AH) originates from
Alternaria
sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treatment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1β, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS-induced nuclear factor-κB (NFκB) DNA-binding activity. Using transfection assay and measurement of an NFκB-sensitive promoter region, we found that transfection of toll-like receptor 4 (TLR4) increased LPS-induced NFκB transcription activity in 293T cells. AH significantly blocked LPS-induced NFκB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFκB signaling pathway.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>23139166</pmid><doi>10.1007/s11010-012-1502-9</doi><tpages>8</tpages></addata></record> |
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| ispartof | Molecular and cellular biochemistry, 2013-02, Vol.374 (1-2), p.29-36 |
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| source | MEDLINE; SpringerNature Journals |
| subjects | AKT protein Alternaria Alternaria - metabolism Animals Anti-Inflammatory Agents - pharmacology Biochemistry Biomedical and Life Sciences Cardiology Cell Line Cell Survival COX-2 inhibitors Cyclooxygenase 2 - metabolism DNA DNA-Binding Proteins - metabolism Enzyme Activation - drug effects Enzymes Genetic research HEK293 Cells Humans Infection Inflammation - immunology Interleukin-1beta - metabolism Interleukin-6 - metabolism Life Sciences Lipopolysaccharides Macrophages - metabolism Medical Biochemistry Mice Mitogens Mycotoxins - pharmacology NF-kappa B - metabolism Nitric oxide Nitric Oxide - biosynthesis Nitric Oxide Synthase Type II - metabolism Oncology p38 Mitogen-Activated Protein Kinases - metabolism Proto-Oncogene Proteins c-akt - metabolism Signal Transduction T cells Toll-Like Receptor 4 - genetics Toll-Like Receptor 4 - metabolism |
| title | Toll-like receptor 4/nuclear factor-κB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect |
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