Inhibitory Effects of a Rice Hull Constituent on Tumor Necrosis Factor α, Prostaglandin E2, and Cyclooxygenase-2 Production in Lipopolysaccharide-Activated Mouse Macrophages
: Isovitexin, isolated from rice hull of Oryza sativa, has been characterized as a potent antioxidant. Its antioxidant activity, determined on the basis of inhibition of lipid peroxidation by the Fenton reaction, was comparable with that of α‐tocopherol, a well‐established antioxidant. Isovitexin wa...
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Veröffentlicht in: | Annals of the New York Academy of Sciences 2005-05, Vol.1042 (1), p.387-395 |
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creator | HUANG, SHENG-TUNG CHEN, CHIEN-TSU CHIENG, KUR-TA HUANG, SHIH-HAO CHIANG, BEEN-HUANG WANG, LENG-FANG KUO, HSIEN-SAW LIN, CHUN-MAO |
description | : Isovitexin, isolated from rice hull of Oryza sativa, has been characterized as a potent antioxidant. Its antioxidant activity, determined on the basis of inhibition of lipid peroxidation by the Fenton reaction, was comparable with that of α‐tocopherol, a well‐established antioxidant. Isovitexin was able to reduce the amount of hydrogen peroxide production induced by lipopolysaccharide (LPS) in mouse macrophage RAW264.7 cells. In this study, we assessed its effects on the production of tumor necrosis factor α (TNF‐α), prostaglandin E2 (PGE2), and the expression of cyclooxygenase‐2 (COX‐2) in LPS‐activated RAW 264.7 macrophages. Isovitexin inhibited the release of TNF‐α, a proinflammatory cytokine, upon LPS activation with a 50% inhibitory concentration (IC50) of 78.6 μM. Isovitexin markedly reduced LPS‐stimulated PGE2 production in a concentration‐dependent manner, with an IC50 of 80.0 μM. The expression of COX‐2 was also inhibited by isovitexin treatment. Our results suggest that suppression of ROS‐mediated COX‐2 expression by isovitexin is beneficial in reducing inflammation and carcinogenesis. |
doi_str_mv | 10.1196/annals.1338.059 |
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Its antioxidant activity, determined on the basis of inhibition of lipid peroxidation by the Fenton reaction, was comparable with that of α‐tocopherol, a well‐established antioxidant. Isovitexin was able to reduce the amount of hydrogen peroxide production induced by lipopolysaccharide (LPS) in mouse macrophage RAW264.7 cells. In this study, we assessed its effects on the production of tumor necrosis factor α (TNF‐α), prostaglandin E2 (PGE2), and the expression of cyclooxygenase‐2 (COX‐2) in LPS‐activated RAW 264.7 macrophages. Isovitexin inhibited the release of TNF‐α, a proinflammatory cytokine, upon LPS activation with a 50% inhibitory concentration (IC50) of 78.6 μM. Isovitexin markedly reduced LPS‐stimulated PGE2 production in a concentration‐dependent manner, with an IC50 of 80.0 μM. The expression of COX‐2 was also inhibited by isovitexin treatment. Our results suggest that suppression of ROS‐mediated COX‐2 expression by isovitexin is beneficial in reducing inflammation and carcinogenesis.</description><identifier>ISSN: 0077-8923</identifier><identifier>EISSN: 1749-6632</identifier><identifier>DOI: 10.1196/annals.1338.059</identifier><identifier>PMID: 15965085</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; antioxidant ; Antioxidants - pharmacology ; Apigenin - pharmacology ; Cell Line ; COX-2 ; Cyclooxygenase 2 - biosynthesis ; Dinoprostone - biosynthesis ; inflammation ; isovitexin ; Lipopolysaccharides - pharmacology ; Macrophages - drug effects ; Macrophages - metabolism ; Mice ; Oryza - chemistry ; Oryza sativa ; PGE2 ; tumor necrosis factor ; Tumor Necrosis Factor-alpha - biosynthesis</subject><ispartof>Annals of the New York Academy of Sciences, 2005-05, Vol.1042 (1), p.387-395</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4837-99e8ef1a92d4fb0e6ce226026468b0fd6478b0391bb77a59cf5849e9222730293</citedby><cites>FETCH-LOGICAL-c4837-99e8ef1a92d4fb0e6ce226026468b0fd6478b0391bb77a59cf5849e9222730293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1196%2Fannals.1338.059$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1196%2Fannals.1338.059$$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/15965085$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HUANG, SHENG-TUNG</creatorcontrib><creatorcontrib>CHEN, CHIEN-TSU</creatorcontrib><creatorcontrib>CHIENG, KUR-TA</creatorcontrib><creatorcontrib>HUANG, SHIH-HAO</creatorcontrib><creatorcontrib>CHIANG, BEEN-HUANG</creatorcontrib><creatorcontrib>WANG, LENG-FANG</creatorcontrib><creatorcontrib>KUO, HSIEN-SAW</creatorcontrib><creatorcontrib>LIN, CHUN-MAO</creatorcontrib><title>Inhibitory Effects of a Rice Hull Constituent on Tumor Necrosis Factor α, Prostaglandin E2, and Cyclooxygenase-2 Production in Lipopolysaccharide-Activated Mouse Macrophages</title><title>Annals of the New York Academy of Sciences</title><addtitle>Ann N Y Acad Sci</addtitle><description>: Isovitexin, isolated from rice hull of Oryza sativa, has been characterized as a potent antioxidant. Its antioxidant activity, determined on the basis of inhibition of lipid peroxidation by the Fenton reaction, was comparable with that of α‐tocopherol, a well‐established antioxidant. Isovitexin was able to reduce the amount of hydrogen peroxide production induced by lipopolysaccharide (LPS) in mouse macrophage RAW264.7 cells. In this study, we assessed its effects on the production of tumor necrosis factor α (TNF‐α), prostaglandin E2 (PGE2), and the expression of cyclooxygenase‐2 (COX‐2) in LPS‐activated RAW 264.7 macrophages. Isovitexin inhibited the release of TNF‐α, a proinflammatory cytokine, upon LPS activation with a 50% inhibitory concentration (IC50) of 78.6 μM. Isovitexin markedly reduced LPS‐stimulated PGE2 production in a concentration‐dependent manner, with an IC50 of 80.0 μM. The expression of COX‐2 was also inhibited by isovitexin treatment. Our results suggest that suppression of ROS‐mediated COX‐2 expression by isovitexin is beneficial in reducing inflammation and carcinogenesis.</description><subject>Animals</subject><subject>antioxidant</subject><subject>Antioxidants - pharmacology</subject><subject>Apigenin - pharmacology</subject><subject>Cell Line</subject><subject>COX-2</subject><subject>Cyclooxygenase 2 - biosynthesis</subject><subject>Dinoprostone - biosynthesis</subject><subject>inflammation</subject><subject>isovitexin</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Mice</subject><subject>Oryza - chemistry</subject><subject>Oryza sativa</subject><subject>PGE2</subject><subject>tumor necrosis factor</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><issn>0077-8923</issn><issn>1749-6632</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2O0zAUhSMEYkphzQ55hVhMOv6J7XhZdTrtSG35G4RYWa5z0xrSuMQJTF4KiRfhmXDUCnawupb9nXPv9UmS5wRPCFHiytS1qcKEMJZPMFcPkhGRmUqFYPRhMsJYyjRXlF0kT0L4jDGheSYfJxeEK8FxzkfJj9t677au9U2P5mUJtg3Il8igd84CWnZVhWa-Dq1rO6hb5Gt01x18gzZgGx9cQDfGRjH69fMSvYk3rdlVpi5cjeb0EsUTmvW28v6-30FtAqR0wIrOti56RWzljv7oqz4Ya_emcQWk0_j4zbRQoLXvAqC1ib2Oe7OD8DR5VMaF4dm5jpMPN_O72TJdvV7czqar1GY5k6lSkENJjKJFVm4xCAuUCkxFJvItLguRyViZItutlIYrW_I8U6AopZJhqtg4eXnyPTb-aweh1QcXLFRxN4gzaSIZzwd4nLz6N8gJZZQLwSN6dUKHnwsNlPrYuINpek2wHtLUpzT1kKaOaUbFi7N5tz1A8Zc_xxeB7AR8dxX0__PTm0_T9ywfhk5PMhdauP8jM80XLSSTXH_cLPT6WuV8vXirl-w3Ni--og</recordid><startdate>200505</startdate><enddate>200505</enddate><creator>HUANG, SHENG-TUNG</creator><creator>CHEN, CHIEN-TSU</creator><creator>CHIENG, KUR-TA</creator><creator>HUANG, SHIH-HAO</creator><creator>CHIANG, BEEN-HUANG</creator><creator>WANG, LENG-FANG</creator><creator>KUO, HSIEN-SAW</creator><creator>LIN, CHUN-MAO</creator><general>Blackwell Publishing Ltd</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>7T5</scope><scope>H94</scope><scope>F1W</scope><scope>H96</scope><scope>L.G</scope></search><sort><creationdate>200505</creationdate><title>Inhibitory Effects of a Rice Hull Constituent on Tumor Necrosis Factor α, Prostaglandin E2, and Cyclooxygenase-2 Production in Lipopolysaccharide-Activated Mouse Macrophages</title><author>HUANG, SHENG-TUNG ; CHEN, CHIEN-TSU ; CHIENG, KUR-TA ; HUANG, SHIH-HAO ; CHIANG, BEEN-HUANG ; WANG, LENG-FANG ; KUO, HSIEN-SAW ; LIN, CHUN-MAO</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4837-99e8ef1a92d4fb0e6ce226026468b0fd6478b0391bb77a59cf5849e9222730293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>antioxidant</topic><topic>Antioxidants - pharmacology</topic><topic>Apigenin - pharmacology</topic><topic>Cell Line</topic><topic>COX-2</topic><topic>Cyclooxygenase 2 - biosynthesis</topic><topic>Dinoprostone - biosynthesis</topic><topic>inflammation</topic><topic>isovitexin</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>Oryza - chemistry</topic><topic>Oryza sativa</topic><topic>PGE2</topic><topic>tumor necrosis factor</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HUANG, SHENG-TUNG</creatorcontrib><creatorcontrib>CHEN, CHIEN-TSU</creatorcontrib><creatorcontrib>CHIENG, KUR-TA</creatorcontrib><creatorcontrib>HUANG, SHIH-HAO</creatorcontrib><creatorcontrib>CHIANG, BEEN-HUANG</creatorcontrib><creatorcontrib>WANG, LENG-FANG</creatorcontrib><creatorcontrib>KUO, HSIEN-SAW</creatorcontrib><creatorcontrib>LIN, CHUN-MAO</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 2: Ocean Technology, Policy & Non-Living Resources</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><jtitle>Annals of the New York Academy of Sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HUANG, SHENG-TUNG</au><au>CHEN, CHIEN-TSU</au><au>CHIENG, KUR-TA</au><au>HUANG, SHIH-HAO</au><au>CHIANG, BEEN-HUANG</au><au>WANG, LENG-FANG</au><au>KUO, HSIEN-SAW</au><au>LIN, CHUN-MAO</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibitory Effects of a Rice Hull Constituent on Tumor Necrosis Factor α, Prostaglandin E2, and Cyclooxygenase-2 Production in Lipopolysaccharide-Activated Mouse Macrophages</atitle><jtitle>Annals of the New York Academy of Sciences</jtitle><addtitle>Ann N Y Acad Sci</addtitle><date>2005-05</date><risdate>2005</risdate><volume>1042</volume><issue>1</issue><spage>387</spage><epage>395</epage><pages>387-395</pages><issn>0077-8923</issn><eissn>1749-6632</eissn><abstract>: Isovitexin, isolated from rice hull of Oryza sativa, has been characterized as a potent antioxidant. Its antioxidant activity, determined on the basis of inhibition of lipid peroxidation by the Fenton reaction, was comparable with that of α‐tocopherol, a well‐established antioxidant. Isovitexin was able to reduce the amount of hydrogen peroxide production induced by lipopolysaccharide (LPS) in mouse macrophage RAW264.7 cells. In this study, we assessed its effects on the production of tumor necrosis factor α (TNF‐α), prostaglandin E2 (PGE2), and the expression of cyclooxygenase‐2 (COX‐2) in LPS‐activated RAW 264.7 macrophages. Isovitexin inhibited the release of TNF‐α, a proinflammatory cytokine, upon LPS activation with a 50% inhibitory concentration (IC50) of 78.6 μM. Isovitexin markedly reduced LPS‐stimulated PGE2 production in a concentration‐dependent manner, with an IC50 of 80.0 μM. The expression of COX‐2 was also inhibited by isovitexin treatment. Our results suggest that suppression of ROS‐mediated COX‐2 expression by isovitexin is beneficial in reducing inflammation and carcinogenesis.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>15965085</pmid><doi>10.1196/annals.1338.059</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals antioxidant Antioxidants - pharmacology Apigenin - pharmacology Cell Line COX-2 Cyclooxygenase 2 - biosynthesis Dinoprostone - biosynthesis inflammation isovitexin Lipopolysaccharides - pharmacology Macrophages - drug effects Macrophages - metabolism Mice Oryza - chemistry Oryza sativa PGE2 tumor necrosis factor Tumor Necrosis Factor-alpha - biosynthesis |
title | Inhibitory Effects of a Rice Hull Constituent on Tumor Necrosis Factor α, Prostaglandin E2, and Cyclooxygenase-2 Production in Lipopolysaccharide-Activated Mouse Macrophages |
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