Forsythoside B Protects Against Experimental Sepsis by Modulating Inflammatory Factors
The present study investigated the effects of Forsythoside B on an experimental model of sepsis induced by caecal ligation and puncture (CLP) in rats and elucidated the potential mechanism in cultured RAW 264.7 cells. Results showed that Forsythoside B concentration‐dependently down‐regulated the le...
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| Veröffentlicht in: | Phytotherapy research 2012-07, Vol.26 (7), p.981-987 |
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| creator | Jiang, Wang-Lin Yong-Xu Zhang, Shu-Ping Zhu, Hai-Bo Jian-Hou |
| description | The present study investigated the effects of Forsythoside B on an experimental model of sepsis induced by caecal ligation and puncture (CLP) in rats and elucidated the potential mechanism in cultured RAW 264.7 cells. Results showed that Forsythoside B concentration‐dependently down‐regulated the levels of TNF‐α, IL‐6 and high‐mobility group‐box 1 protein (HMGB1) in lipopolysaccharide (LPS)‐stimulated RAW264.7 cells, inhibited the IκB kinase (IKK) pathway and modulated nuclear factor (NF)‐ κB. Intravenous injection (i.v.) of Forsythoside B alone or plus Imipenem reduced serum levels of TNF‐α, IL‐6, HMGB1, triggering receptor expressed on myeloid cells (TREM‐1) and endotoxin, while the serum level of IL‐10 was up‐regulated and myeloperoxidase (MPO) in lung, liver and small intestine was reduced. Meanwhile, i.v. of Forsythoside B alone or plus Imipenem reduced CLP‐induced lethality in rats. These data indicated that the antisepsis effect of Forsythoside B is mediated by decreasing local and systemic levels of a wide spectrum of inflammatory mediators. Its antisepsis mechanism may be that Forsythoside B binds to LPS and reduces the biological activity of serum LPS, and inhibits NF‐κB activition. Our studies enhance the case for the use of Forsythoside B in sepsis. Forsythoside B itself has promise as a therapy for the treatment of sepsis in humans. Copyright © 2011 John Wiley & Sons, Ltd. |
| doi_str_mv | 10.1002/ptr.3668 |
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Results showed that Forsythoside B concentration‐dependently down‐regulated the levels of TNF‐α, IL‐6 and high‐mobility group‐box 1 protein (HMGB1) in lipopolysaccharide (LPS)‐stimulated RAW264.7 cells, inhibited the IκB kinase (IKK) pathway and modulated nuclear factor (NF)‐ κB. Intravenous injection (i.v.) of Forsythoside B alone or plus Imipenem reduced serum levels of TNF‐α, IL‐6, HMGB1, triggering receptor expressed on myeloid cells (TREM‐1) and endotoxin, while the serum level of IL‐10 was up‐regulated and myeloperoxidase (MPO) in lung, liver and small intestine was reduced. Meanwhile, i.v. of Forsythoside B alone or plus Imipenem reduced CLP‐induced lethality in rats. These data indicated that the antisepsis effect of Forsythoside B is mediated by decreasing local and systemic levels of a wide spectrum of inflammatory mediators. Its antisepsis mechanism may be that Forsythoside B binds to LPS and reduces the biological activity of serum LPS, and inhibits NF‐κB activition. Our studies enhance the case for the use of Forsythoside B in sepsis. Forsythoside B itself has promise as a therapy for the treatment of sepsis in humans. Copyright © 2011 John Wiley & Sons, Ltd.</description><identifier>ISSN: 0951-418X</identifier><identifier>EISSN: 1099-1573</identifier><identifier>DOI: 10.1002/ptr.3668</identifier><identifier>PMID: 22147417</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Animals ; Biological and medical sciences ; caecal ligation and puncture ; Caffeic Acids - pharmacology ; Cell Line ; Forsythoside B ; General pharmacology ; Glucosides - pharmacology ; HMGB1 Protein - metabolism ; I-kappa B Kinase - metabolism ; IL-10 ; Imipenem - pharmacology ; Inflammation Mediators - metabolism ; Interleukin-10 - blood ; Interleukin-6 - metabolism ; Intestine, Small - drug effects ; Lipopolysaccharides - pharmacology ; Liver - drug effects ; Lung - drug effects ; Male ; Medical sciences ; Mice ; NF-kappa B - metabolism ; NF-κB ; Peroxidase - metabolism ; Pharmacognosy. Homeopathy. Health food ; Pharmacology. Drug treatments ; Rats ; Rats, Sprague-Dawley ; Receptors, Immunologic - metabolism ; Sepsis - drug therapy ; septic shock ; triggering receptor expressed on myeloid cells ; Triggering Receptor Expressed on Myeloid Cells-1 ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Phytotherapy research, 2012-07, Vol.26 (7), p.981-987</ispartof><rights>Copyright © 2011 John Wiley & Sons, Ltd.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4238-b02d1be8d19a7da54c040b6626f16d972a59f8899762b606330e827085729e623</citedby><cites>FETCH-LOGICAL-c4238-b02d1be8d19a7da54c040b6626f16d972a59f8899762b606330e827085729e623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fptr.3668$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fptr.3668$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26136590$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22147417$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Wang-Lin</creatorcontrib><creatorcontrib>Yong-Xu</creatorcontrib><creatorcontrib>Zhang, Shu-Ping</creatorcontrib><creatorcontrib>Zhu, Hai-Bo</creatorcontrib><creatorcontrib>Jian-Hou</creatorcontrib><title>Forsythoside B Protects Against Experimental Sepsis by Modulating Inflammatory Factors</title><title>Phytotherapy research</title><addtitle>Phytother. Res</addtitle><description>The present study investigated the effects of Forsythoside B on an experimental model of sepsis induced by caecal ligation and puncture (CLP) in rats and elucidated the potential mechanism in cultured RAW 264.7 cells. Results showed that Forsythoside B concentration‐dependently down‐regulated the levels of TNF‐α, IL‐6 and high‐mobility group‐box 1 protein (HMGB1) in lipopolysaccharide (LPS)‐stimulated RAW264.7 cells, inhibited the IκB kinase (IKK) pathway and modulated nuclear factor (NF)‐ κB. Intravenous injection (i.v.) of Forsythoside B alone or plus Imipenem reduced serum levels of TNF‐α, IL‐6, HMGB1, triggering receptor expressed on myeloid cells (TREM‐1) and endotoxin, while the serum level of IL‐10 was up‐regulated and myeloperoxidase (MPO) in lung, liver and small intestine was reduced. Meanwhile, i.v. of Forsythoside B alone or plus Imipenem reduced CLP‐induced lethality in rats. These data indicated that the antisepsis effect of Forsythoside B is mediated by decreasing local and systemic levels of a wide spectrum of inflammatory mediators. Its antisepsis mechanism may be that Forsythoside B binds to LPS and reduces the biological activity of serum LPS, and inhibits NF‐κB activition. Our studies enhance the case for the use of Forsythoside B in sepsis. Forsythoside B itself has promise as a therapy for the treatment of sepsis in humans. Copyright © 2011 John Wiley & Sons, Ltd.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>caecal ligation and puncture</subject><subject>Caffeic Acids - pharmacology</subject><subject>Cell Line</subject><subject>Forsythoside B</subject><subject>General pharmacology</subject><subject>Glucosides - pharmacology</subject><subject>HMGB1 Protein - metabolism</subject><subject>I-kappa B Kinase - metabolism</subject><subject>IL-10</subject><subject>Imipenem - pharmacology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin-10 - blood</subject><subject>Interleukin-6 - metabolism</subject><subject>Intestine, Small - drug effects</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Liver - drug effects</subject><subject>Lung - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>Peroxidase - metabolism</subject><subject>Pharmacognosy. Homeopathy. Health food</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Immunologic - metabolism</subject><subject>Sepsis - drug therapy</subject><subject>septic shock</subject><subject>triggering receptor expressed on myeloid cells</subject><subject>Triggering Receptor Expressed on Myeloid Cells-1</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0951-418X</issn><issn>1099-1573</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10EtPFEEUBeCK0ciIJv4C0xsTN423Hl2PJRJmIBmRICq7SnV3NZb2i7o1gf73NKGFlauz-XJP7iHkPYUDCsA-jykecCn1C7KiYExOC8VfkhWYguaC6qs98gbxDwAYBuI12WOMCiWoWpGf6yHilH4PGGqffcnO45B8lTA7vHahx5Qd340-hs73ybXZdz9iwKycsq9DvWtdCv11dto3res6l4Y4ZWtXzYlvyavGtejfLblPfqyPL49O8u23zenR4TavBOM6L4HVtPS6psap2hWiAgGllEw2VNZGMVeYRmtjlGSlBMk5eM0U6EIx4yXj--TT490xDjc7j8l2ASvftq73ww4tBSbACKD8mVZxQIy-seP8l4vTjOzDinZe0T6sONMPy9Vd2fn6Cf6bbQYfF-Cwcm0TXV8FfHaSclkYmF3-6G5D66f_Ftrzy4ulePEBk7978i7-tVJxVdhfZxurzy6utNls7Qm_Bzr4lsc</recordid><startdate>201207</startdate><enddate>201207</enddate><creator>Jiang, Wang-Lin</creator><creator>Yong-Xu</creator><creator>Zhang, Shu-Ping</creator><creator>Zhu, Hai-Bo</creator><creator>Jian-Hou</creator><general>John Wiley & Sons, Ltd</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</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>7X8</scope></search><sort><creationdate>201207</creationdate><title>Forsythoside B Protects Against Experimental Sepsis by Modulating Inflammatory Factors</title><author>Jiang, Wang-Lin ; Yong-Xu ; Zhang, Shu-Ping ; Zhu, Hai-Bo ; Jian-Hou</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4238-b02d1be8d19a7da54c040b6626f16d972a59f8899762b606330e827085729e623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>caecal ligation and puncture</topic><topic>Caffeic Acids - pharmacology</topic><topic>Cell Line</topic><topic>Forsythoside B</topic><topic>General pharmacology</topic><topic>Glucosides - pharmacology</topic><topic>HMGB1 Protein - metabolism</topic><topic>I-kappa B Kinase - metabolism</topic><topic>IL-10</topic><topic>Imipenem - pharmacology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin-10 - blood</topic><topic>Interleukin-6 - metabolism</topic><topic>Intestine, Small - drug effects</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Liver - drug effects</topic><topic>Lung - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>Peroxidase - metabolism</topic><topic>Pharmacognosy. Homeopathy. Health food</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Immunologic - metabolism</topic><topic>Sepsis - drug therapy</topic><topic>septic shock</topic><topic>triggering receptor expressed on myeloid cells</topic><topic>Triggering Receptor Expressed on Myeloid Cells-1</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Wang-Lin</creatorcontrib><creatorcontrib>Yong-Xu</creatorcontrib><creatorcontrib>Zhang, Shu-Ping</creatorcontrib><creatorcontrib>Zhu, Hai-Bo</creatorcontrib><creatorcontrib>Jian-Hou</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Phytotherapy research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Wang-Lin</au><au>Yong-Xu</au><au>Zhang, Shu-Ping</au><au>Zhu, Hai-Bo</au><au>Jian-Hou</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Forsythoside B Protects Against Experimental Sepsis by Modulating Inflammatory Factors</atitle><jtitle>Phytotherapy research</jtitle><addtitle>Phytother. Res</addtitle><date>2012-07</date><risdate>2012</risdate><volume>26</volume><issue>7</issue><spage>981</spage><epage>987</epage><pages>981-987</pages><issn>0951-418X</issn><eissn>1099-1573</eissn><abstract>The present study investigated the effects of Forsythoside B on an experimental model of sepsis induced by caecal ligation and puncture (CLP) in rats and elucidated the potential mechanism in cultured RAW 264.7 cells. Results showed that Forsythoside B concentration‐dependently down‐regulated the levels of TNF‐α, IL‐6 and high‐mobility group‐box 1 protein (HMGB1) in lipopolysaccharide (LPS)‐stimulated RAW264.7 cells, inhibited the IκB kinase (IKK) pathway and modulated nuclear factor (NF)‐ κB. Intravenous injection (i.v.) of Forsythoside B alone or plus Imipenem reduced serum levels of TNF‐α, IL‐6, HMGB1, triggering receptor expressed on myeloid cells (TREM‐1) and endotoxin, while the serum level of IL‐10 was up‐regulated and myeloperoxidase (MPO) in lung, liver and small intestine was reduced. Meanwhile, i.v. of Forsythoside B alone or plus Imipenem reduced CLP‐induced lethality in rats. These data indicated that the antisepsis effect of Forsythoside B is mediated by decreasing local and systemic levels of a wide spectrum of inflammatory mediators. Its antisepsis mechanism may be that Forsythoside B binds to LPS and reduces the biological activity of serum LPS, and inhibits NF‐κB activition. Our studies enhance the case for the use of Forsythoside B in sepsis. Forsythoside B itself has promise as a therapy for the treatment of sepsis in humans. Copyright © 2011 John Wiley & Sons, Ltd.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>22147417</pmid><doi>10.1002/ptr.3668</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences caecal ligation and puncture Caffeic Acids - pharmacology Cell Line Forsythoside B General pharmacology Glucosides - pharmacology HMGB1 Protein - metabolism I-kappa B Kinase - metabolism IL-10 Imipenem - pharmacology Inflammation Mediators - metabolism Interleukin-10 - blood Interleukin-6 - metabolism Intestine, Small - drug effects Lipopolysaccharides - pharmacology Liver - drug effects Lung - drug effects Male Medical sciences Mice NF-kappa B - metabolism NF-κB Peroxidase - metabolism Pharmacognosy. Homeopathy. Health food Pharmacology. Drug treatments Rats Rats, Sprague-Dawley Receptors, Immunologic - metabolism Sepsis - drug therapy septic shock triggering receptor expressed on myeloid cells Triggering Receptor Expressed on Myeloid Cells-1 Tumor Necrosis Factor-alpha - metabolism |
| title | Forsythoside B Protects Against Experimental Sepsis by Modulating Inflammatory Factors |
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