Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation
Astragalin, a bioactive component isolated from Rosa agrestis, has been described to exhibit anti-inflammatory activity. The aim of this study was to investigate the anti-inflammatory effects and the underlying mechanisms of astragalin on IL-1β-stimulated human osteoarthritis chondrocyte. The produc...
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| Veröffentlicht in: | International immunopharmacology 2015-03, Vol.25 (1), p.83-87 |
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| creator | Ma, Zhiqiang Piao, Taikui Wang, Yanlong Liu, Jianyu |
| description | Astragalin, a bioactive component isolated from Rosa agrestis, has been described to exhibit anti-inflammatory activity. The aim of this study was to investigate the anti-inflammatory effects and the underlying mechanisms of astragalin on IL-1β-stimulated human osteoarthritis chondrocyte. The production of NO and PGE2 was detected by Griess reaction and ELISA. The expression of iNOS and COX-2 was detected by western blotting. The expression of NF-κB and MAPKs was detected by western blot analysis. We found that astragalin dose-dependently inhibited IL-1β-induced NO and PGE2 production, as well as iNOS and COX-2 expression. Meanwhile, western blot analysis showed that astragalin inhibited IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte. In addition, astragalin was found to activate PPAR-γ. The inhibition of astragalin on IL-1β-induced NO and PGE2 production can be reversed by PPAR-γ antagonist GW9662. Astragalin suppressed IL-1β-induced inflammatory mediators via activating PPAR-γ, which subsequently inhibited IL-1β-induced NF-κB and MAPK activation. Astragalin may be a potential agent in the treatment of osteoarthritis.
•Astragalin inhibits IL-1β-induced NO and PGE2 production.•Astragalin suppresses the expression iNOS and COX-2 both in mRNA and protein levels.•Astragalin inhibits IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte. |
| doi_str_mv | 10.1016/j.intimp.2015.01.018 |
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•Astragalin inhibits IL-1β-induced NO and PGE2 production.•Astragalin suppresses the expression iNOS and COX-2 both in mRNA and protein levels.•Astragalin inhibits IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2015.01.018</identifier><identifier>PMID: 25637445</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Adult ; Aged ; Anilides - pharmacology ; Anti-Inflammatory Agents - pharmacology ; Astragalin ; Cells, Cultured ; Chondrocytes - drug effects ; Chondrocytes - immunology ; Cyclooxygenase 2 - genetics ; Cyclooxygenase 2 - metabolism ; Dinoprostone - metabolism ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Humans ; IL-1β ; Interleukin-1beta - immunology ; Kaempferols - pharmacology ; Middle Aged ; NF-kappa B - metabolism ; NF-κB ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Osteoarthritis ; Osteoarthritis - drug therapy ; Osteoarthritis - immunology ; PPAR gamma - antagonists & inhibitors ; Rosa - immunology ; Transcriptional Activation - drug effects</subject><ispartof>International immunopharmacology, 2015-03, Vol.25 (1), p.83-87</ispartof><rights>2015</rights><rights>Copyright © 2015. Published by Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c413t-1d13bfba224e4b1eb098f5bad2c3a6fd7d324e313e8204462865439847712c913</citedby><cites>FETCH-LOGICAL-c413t-1d13bfba224e4b1eb098f5bad2c3a6fd7d324e313e8204462865439847712c913</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1567576915000259$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25637445$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Zhiqiang</creatorcontrib><creatorcontrib>Piao, Taikui</creatorcontrib><creatorcontrib>Wang, Yanlong</creatorcontrib><creatorcontrib>Liu, Jianyu</creatorcontrib><title>Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>Astragalin, a bioactive component isolated from Rosa agrestis, has been described to exhibit anti-inflammatory activity. The aim of this study was to investigate the anti-inflammatory effects and the underlying mechanisms of astragalin on IL-1β-stimulated human osteoarthritis chondrocyte. The production of NO and PGE2 was detected by Griess reaction and ELISA. The expression of iNOS and COX-2 was detected by western blotting. The expression of NF-κB and MAPKs was detected by western blot analysis. We found that astragalin dose-dependently inhibited IL-1β-induced NO and PGE2 production, as well as iNOS and COX-2 expression. Meanwhile, western blot analysis showed that astragalin inhibited IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte. In addition, astragalin was found to activate PPAR-γ. The inhibition of astragalin on IL-1β-induced NO and PGE2 production can be reversed by PPAR-γ antagonist GW9662. Astragalin suppressed IL-1β-induced inflammatory mediators via activating PPAR-γ, which subsequently inhibited IL-1β-induced NF-κB and MAPK activation. Astragalin may be a potential agent in the treatment of osteoarthritis.
•Astragalin inhibits IL-1β-induced NO and PGE2 production.•Astragalin suppresses the expression iNOS and COX-2 both in mRNA and protein levels.•Astragalin inhibits IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte.</description><subject>Adult</subject><subject>Aged</subject><subject>Anilides - pharmacology</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Astragalin</subject><subject>Cells, Cultured</subject><subject>Chondrocytes - drug effects</subject><subject>Chondrocytes - immunology</subject><subject>Cyclooxygenase 2 - genetics</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Dinoprostone - metabolism</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Interleukin-1beta - immunology</subject><subject>Kaempferols - pharmacology</subject><subject>Middle Aged</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Osteoarthritis</subject><subject>Osteoarthritis - drug therapy</subject><subject>Osteoarthritis - immunology</subject><subject>PPAR gamma - antagonists & inhibitors</subject><subject>Rosa - immunology</subject><subject>Transcriptional Activation - drug effects</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UcFu1DAQtRCIlsIfIOQjlyye2I6TC9JS0VKxtBzgbDm20_UqsRfbqbSfwa9w7Ef0m3C0LUekkWY0894bzTyE3gJZAYHmw27lfHbTflUT4CsCJdpn6BRa0VYgCH9eat6IioumO0GvUtoRUvoMXqKTmjdUMMZP0e91ylHdqtF57PzW9S4nfLWp4OFP5byZtTWlP4xqmlQO8YAna9xSJbyPocyzCwsTb-dJeRxStkHFvI0uu4T1NngTgz5ki_vD0wLnb_H1RfVw_wkrb_C39fevWBWhO7WIvUYvBjUm--Yxn6GfF59_nH-pNjeXV-frTaUZ0FyBAdoPvaprZlkPtiddO_BemVpT1QxGGFomFKhta8JYU7cNZ7RrmRBQ6w7oGXp_1C13_JptynJySdtxVN6GOUloBCVC8I4WKDtCdQwpRTvIfXSTigcJRC5myJ08miEXMySBEm2hvXvcMPflbf9IT98vgI9HgC133jkbZdLO-vJzF63O0gT3_w1_AbBpoK4</recordid><startdate>20150301</startdate><enddate>20150301</enddate><creator>Ma, Zhiqiang</creator><creator>Piao, Taikui</creator><creator>Wang, Yanlong</creator><creator>Liu, Jianyu</creator><general>Elsevier B.V</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>7X8</scope></search><sort><creationdate>20150301</creationdate><title>Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation</title><author>Ma, Zhiqiang ; Piao, Taikui ; Wang, Yanlong ; Liu, Jianyu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-1d13bfba224e4b1eb098f5bad2c3a6fd7d324e313e8204462865439847712c913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Anilides - pharmacology</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Astragalin</topic><topic>Cells, Cultured</topic><topic>Chondrocytes - drug effects</topic><topic>Chondrocytes - immunology</topic><topic>Cyclooxygenase 2 - genetics</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Dinoprostone - metabolism</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Humans</topic><topic>IL-1β</topic><topic>Interleukin-1beta - immunology</topic><topic>Kaempferols - pharmacology</topic><topic>Middle Aged</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Osteoarthritis</topic><topic>Osteoarthritis - drug therapy</topic><topic>Osteoarthritis - immunology</topic><topic>PPAR gamma - antagonists & inhibitors</topic><topic>Rosa - immunology</topic><topic>Transcriptional Activation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Zhiqiang</creatorcontrib><creatorcontrib>Piao, Taikui</creatorcontrib><creatorcontrib>Wang, Yanlong</creatorcontrib><creatorcontrib>Liu, Jianyu</creatorcontrib><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>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Zhiqiang</au><au>Piao, Taikui</au><au>Wang, Yanlong</au><au>Liu, Jianyu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2015-03-01</date><risdate>2015</risdate><volume>25</volume><issue>1</issue><spage>83</spage><epage>87</epage><pages>83-87</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>Astragalin, a bioactive component isolated from Rosa agrestis, has been described to exhibit anti-inflammatory activity. The aim of this study was to investigate the anti-inflammatory effects and the underlying mechanisms of astragalin on IL-1β-stimulated human osteoarthritis chondrocyte. The production of NO and PGE2 was detected by Griess reaction and ELISA. The expression of iNOS and COX-2 was detected by western blotting. The expression of NF-κB and MAPKs was detected by western blot analysis. We found that astragalin dose-dependently inhibited IL-1β-induced NO and PGE2 production, as well as iNOS and COX-2 expression. Meanwhile, western blot analysis showed that astragalin inhibited IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte. In addition, astragalin was found to activate PPAR-γ. The inhibition of astragalin on IL-1β-induced NO and PGE2 production can be reversed by PPAR-γ antagonist GW9662. Astragalin suppressed IL-1β-induced inflammatory mediators via activating PPAR-γ, which subsequently inhibited IL-1β-induced NF-κB and MAPK activation. Astragalin may be a potential agent in the treatment of osteoarthritis.
•Astragalin inhibits IL-1β-induced NO and PGE2 production.•Astragalin suppresses the expression iNOS and COX-2 both in mRNA and protein levels.•Astragalin inhibits IL-1β-induced NF-κB and MAPK activation in human osteoarthritis chondrocyte.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>25637445</pmid><doi>10.1016/j.intimp.2015.01.018</doi><tpages>5</tpages></addata></record> |
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| subjects | Adult Aged Anilides - pharmacology Anti-Inflammatory Agents - pharmacology Astragalin Cells, Cultured Chondrocytes - drug effects Chondrocytes - immunology Cyclooxygenase 2 - genetics Cyclooxygenase 2 - metabolism Dinoprostone - metabolism Extracellular Signal-Regulated MAP Kinases - metabolism Humans IL-1β Interleukin-1beta - immunology Kaempferols - pharmacology Middle Aged NF-kappa B - metabolism NF-κB Nitric Oxide - metabolism Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Osteoarthritis Osteoarthritis - drug therapy Osteoarthritis - immunology PPAR gamma - antagonists & inhibitors Rosa - immunology Transcriptional Activation - drug effects |
| title | Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation |
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