Astaxanthin suppresses scavenger receptor expression and matrix metalloproteinase activity in macrophages
Background Astaxanthin is a red carotenoid pigment which has significant potential for antioxidant activity. The macrophages in atherosclerotic lesions, known as activated macrophages, express scavenger receptors responsible for the clearance of pathogenic lipoproteins. In addition, the expression a...
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| Veröffentlicht in: | European journal of nutrition 2010-03, Vol.49 (2), p.119-126 |
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| creator | Kishimoto, Yoshimi Tani, Mariko Uto-Kondo, Harumi Iizuka, Maki Saita, Emi Sone, Hirohito Kurata, Hideaki Kondo, Kazuo |
| description | Background Astaxanthin is a red carotenoid pigment which has significant potential for antioxidant activity. The macrophages in atherosclerotic lesions, known as activated macrophages, express scavenger receptors responsible for the clearance of pathogenic lipoproteins. In addition, the expression and secretion of proteolytic enzymes, matrix metalloproteinases (MMPs), and pro-inflammatory cytokines are remarkably promoted in activated macrophages. Aim of the study In this study, we investigated the effects of astaxanthin on the expression of scavenger receptors, MMPs, and pro-inflammatory cytokines in macrophages. Methods THP-1 macrophages were incubated with 5-10 μM astaxanthin for 24 h. The expression levels of scavenger receptors, MMPs, and pro-inflammatory cytokines were determined by Western blot analysis or real-time RT-PCR. The MMP-9 and -2 activities were examined by gelatin zymography and total MMP activity was measured by fluorometry. Results We found that astaxanthin remarkably decreased the class A scavenger receptor and CD36 expression in the protein and mRNA levels. Astaxanthin also reduced MMP-1, -2, -3, -9, -12, and -14 activity and expression. The mRNA expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, inducible nitric oxide synthase, and cyclooxygenase-2 were significantly suppressed by astaxanthin. Furthermore, astaxanthin inhibited the phosphorylation of nuclear factor-κB. Conclusions These results indicate that astaxanthin has inhibitory effects on macrophage activation, such as scavenger receptors up-regulation, MMPs activation, and pro-inflammatory cytokines secretion. |
| doi_str_mv | 10.1007/s00394-009-0056-4 |
| format | Article |
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The macrophages in atherosclerotic lesions, known as activated macrophages, express scavenger receptors responsible for the clearance of pathogenic lipoproteins. In addition, the expression and secretion of proteolytic enzymes, matrix metalloproteinases (MMPs), and pro-inflammatory cytokines are remarkably promoted in activated macrophages. Aim of the study In this study, we investigated the effects of astaxanthin on the expression of scavenger receptors, MMPs, and pro-inflammatory cytokines in macrophages. Methods THP-1 macrophages were incubated with 5-10 μM astaxanthin for 24 h. The expression levels of scavenger receptors, MMPs, and pro-inflammatory cytokines were determined by Western blot analysis or real-time RT-PCR. The MMP-9 and -2 activities were examined by gelatin zymography and total MMP activity was measured by fluorometry. Results We found that astaxanthin remarkably decreased the class A scavenger receptor and CD36 expression in the protein and mRNA levels. Astaxanthin also reduced MMP-1, -2, -3, -9, -12, and -14 activity and expression. The mRNA expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, inducible nitric oxide synthase, and cyclooxygenase-2 were significantly suppressed by astaxanthin. Furthermore, astaxanthin inhibited the phosphorylation of nuclear factor-κB. Conclusions These results indicate that astaxanthin has inhibitory effects on macrophage activation, such as scavenger receptors up-regulation, MMPs activation, and pro-inflammatory cytokines secretion.</description><identifier>ISSN: 1436-6207</identifier><identifier>EISSN: 1436-6215</identifier><identifier>DOI: 10.1007/s00394-009-0056-4</identifier><identifier>PMID: 19784539</identifier><language>eng</language><publisher>Berlin/Heidelberg: Berlin/Heidelberg : Springer-Verlag</publisher><subject>Antioxidants - pharmacology ; Atherosclerosis - prevention & control ; CD36 Antigens - genetics ; CD36 Antigens - metabolism ; Cell Line ; Chemistry ; Chemistry and Materials Science ; Cyclooxygenase 2 - genetics ; Cyclooxygenase 2 - metabolism ; Enzyme Activation - drug effects ; Gene Expression Regulation ; Humans ; Inflammation Mediators - metabolism ; Isoenzymes - genetics ; Isoenzymes - metabolism ; Macrophage Activation - drug effects ; Macrophages - drug effects ; Macrophages - metabolism ; Matrix Metalloproteinases - genetics ; Matrix Metalloproteinases - metabolism ; NF-kappa B - metabolism ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; Nutrition ; Original Contribution ; Phosphorylation ; Protein Processing, Post-Translational ; RNA, Messenger - metabolism ; Scavenger Receptors, Class A - genetics ; Scavenger Receptors, Class A - metabolism ; Xanthophylls - pharmacology</subject><ispartof>European journal of nutrition, 2010-03, Vol.49 (2), p.119-126</ispartof><rights>Springer-Verlag 2009</rights><rights>Springer-Verlag 2010</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c460t-9d87fc28f36382068b06272db02147b23787bbd8980d394a1517e0eedff393203</citedby><cites>FETCH-LOGICAL-c460t-9d87fc28f36382068b06272db02147b23787bbd8980d394a1517e0eedff393203</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/s00394-009-0056-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00394-009-0056-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19784539$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kishimoto, Yoshimi</creatorcontrib><creatorcontrib>Tani, Mariko</creatorcontrib><creatorcontrib>Uto-Kondo, Harumi</creatorcontrib><creatorcontrib>Iizuka, Maki</creatorcontrib><creatorcontrib>Saita, Emi</creatorcontrib><creatorcontrib>Sone, Hirohito</creatorcontrib><creatorcontrib>Kurata, Hideaki</creatorcontrib><creatorcontrib>Kondo, Kazuo</creatorcontrib><title>Astaxanthin suppresses scavenger receptor expression and matrix metalloproteinase activity in macrophages</title><title>European journal of nutrition</title><addtitle>Eur J Nutr</addtitle><addtitle>Eur J Nutr</addtitle><description>Background Astaxanthin is a red carotenoid pigment which has significant potential for antioxidant activity. The macrophages in atherosclerotic lesions, known as activated macrophages, express scavenger receptors responsible for the clearance of pathogenic lipoproteins. In addition, the expression and secretion of proteolytic enzymes, matrix metalloproteinases (MMPs), and pro-inflammatory cytokines are remarkably promoted in activated macrophages. Aim of the study In this study, we investigated the effects of astaxanthin on the expression of scavenger receptors, MMPs, and pro-inflammatory cytokines in macrophages. Methods THP-1 macrophages were incubated with 5-10 μM astaxanthin for 24 h. The expression levels of scavenger receptors, MMPs, and pro-inflammatory cytokines were determined by Western blot analysis or real-time RT-PCR. The MMP-9 and -2 activities were examined by gelatin zymography and total MMP activity was measured by fluorometry. Results We found that astaxanthin remarkably decreased the class A scavenger receptor and CD36 expression in the protein and mRNA levels. Astaxanthin also reduced MMP-1, -2, -3, -9, -12, and -14 activity and expression. The mRNA expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, inducible nitric oxide synthase, and cyclooxygenase-2 were significantly suppressed by astaxanthin. Furthermore, astaxanthin inhibited the phosphorylation of nuclear factor-κB. Conclusions These results indicate that astaxanthin has inhibitory effects on macrophage activation, such as scavenger receptors up-regulation, MMPs activation, and pro-inflammatory cytokines secretion.</description><subject>Antioxidants - pharmacology</subject><subject>Atherosclerosis - prevention & control</subject><subject>CD36 Antigens - genetics</subject><subject>CD36 Antigens - metabolism</subject><subject>Cell Line</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Cyclooxygenase 2 - genetics</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Enzyme Activation - drug effects</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Inflammation Mediators - metabolism</subject><subject>Isoenzymes - genetics</subject><subject>Isoenzymes - metabolism</subject><subject>Macrophage Activation - drug effects</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Matrix Metalloproteinases - genetics</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nutrition</subject><subject>Original Contribution</subject><subject>Phosphorylation</subject><subject>Protein Processing, Post-Translational</subject><subject>RNA, Messenger - metabolism</subject><subject>Scavenger Receptors, Class A - genetics</subject><subject>Scavenger Receptors, Class A - metabolism</subject><subject>Xanthophylls - pharmacology</subject><issn>1436-6207</issn><issn>1436-6215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp9kctu1TAQhi1ERS_wAGzAYtNVythObGdZVdykSiyga8tJJqeucsPjVKdvjw85ohILFtZYmm_-ufyMvRVwJQDMRwJQdVkA1PlVuihfsDNRKl1oKaqXf_9gTtk50QMASKXFK3YqamPLStVnLFxT8ns_pfswcVqXJSIREqfWP-K0w8gjtrikOXLc_0mGeeJ-6vjoUwx7PmLywzAvcU4YJk_IfZvCY0hPPCuOvo3zcu93SK_ZSe8HwjfHeMHuPn_6efO1uP3-5dvN9W3RlhpSUXfW9K20vdLKStC2AS2N7BqQojSNVMaapulsbaHLy3tRCYOA2PW9qpUEdcEuN9080q8VKbkxUIvD4CecV3JGqVpqbctMfviHfJjXOOXhXO5lbZX1MiQ2KC9CFLF3Swyjj09OgDu44DYXXHbBHVxwB-F3R-G1GbF7rjiePQNyAyinDld-7vw_1fdbUe9n53cxkLv7IUEoEBaUNaX6DYgunMo</recordid><startdate>20100301</startdate><enddate>20100301</enddate><creator>Kishimoto, Yoshimi</creator><creator>Tani, Mariko</creator><creator>Uto-Kondo, Harumi</creator><creator>Iizuka, Maki</creator><creator>Saita, Emi</creator><creator>Sone, Hirohito</creator><creator>Kurata, Hideaki</creator><creator>Kondo, Kazuo</creator><general>Berlin/Heidelberg : Springer-Verlag</general><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>FBQ</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>3V.</scope><scope>7QP</scope><scope>7RQ</scope><scope>7RV</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20100301</creationdate><title>Astaxanthin suppresses scavenger receptor expression and matrix metalloproteinase activity in macrophages</title><author>Kishimoto, Yoshimi ; Tani, Mariko ; Uto-Kondo, Harumi ; Iizuka, Maki ; Saita, Emi ; Sone, Hirohito ; Kurata, Hideaki ; Kondo, Kazuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c460t-9d87fc28f36382068b06272db02147b23787bbd8980d394a1517e0eedff393203</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Antioxidants - pharmacology</topic><topic>Atherosclerosis - prevention & control</topic><topic>CD36 Antigens - genetics</topic><topic>CD36 Antigens - metabolism</topic><topic>Cell Line</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>Cyclooxygenase 2 - genetics</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Enzyme Activation - drug effects</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Inflammation Mediators - metabolism</topic><topic>Isoenzymes - genetics</topic><topic>Isoenzymes - metabolism</topic><topic>Macrophage Activation - drug effects</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Matrix Metalloproteinases - genetics</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nutrition</topic><topic>Original Contribution</topic><topic>Phosphorylation</topic><topic>Protein Processing, Post-Translational</topic><topic>RNA, Messenger - metabolism</topic><topic>Scavenger Receptors, Class A - genetics</topic><topic>Scavenger Receptors, Class A - metabolism</topic><topic>Xanthophylls - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kishimoto, Yoshimi</creatorcontrib><creatorcontrib>Tani, Mariko</creatorcontrib><creatorcontrib>Uto-Kondo, Harumi</creatorcontrib><creatorcontrib>Iizuka, Maki</creatorcontrib><creatorcontrib>Saita, Emi</creatorcontrib><creatorcontrib>Sone, Hirohito</creatorcontrib><creatorcontrib>Kurata, Hideaki</creatorcontrib><creatorcontrib>Kondo, Kazuo</creatorcontrib><collection>AGRIS</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Career & Technical Education Database</collection><collection>Nursing & Allied Health Database</collection><collection>Physical Education Index</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>ProQuest Public Health Database</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 Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of nutrition</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kishimoto, Yoshimi</au><au>Tani, Mariko</au><au>Uto-Kondo, Harumi</au><au>Iizuka, Maki</au><au>Saita, Emi</au><au>Sone, Hirohito</au><au>Kurata, Hideaki</au><au>Kondo, Kazuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astaxanthin suppresses scavenger receptor expression and matrix metalloproteinase activity in macrophages</atitle><jtitle>European journal of nutrition</jtitle><stitle>Eur J Nutr</stitle><addtitle>Eur J Nutr</addtitle><date>2010-03-01</date><risdate>2010</risdate><volume>49</volume><issue>2</issue><spage>119</spage><epage>126</epage><pages>119-126</pages><issn>1436-6207</issn><eissn>1436-6215</eissn><abstract>Background Astaxanthin is a red carotenoid pigment which has significant potential for antioxidant activity. The macrophages in atherosclerotic lesions, known as activated macrophages, express scavenger receptors responsible for the clearance of pathogenic lipoproteins. In addition, the expression and secretion of proteolytic enzymes, matrix metalloproteinases (MMPs), and pro-inflammatory cytokines are remarkably promoted in activated macrophages. Aim of the study In this study, we investigated the effects of astaxanthin on the expression of scavenger receptors, MMPs, and pro-inflammatory cytokines in macrophages. Methods THP-1 macrophages were incubated with 5-10 μM astaxanthin for 24 h. The expression levels of scavenger receptors, MMPs, and pro-inflammatory cytokines were determined by Western blot analysis or real-time RT-PCR. The MMP-9 and -2 activities were examined by gelatin zymography and total MMP activity was measured by fluorometry. Results We found that astaxanthin remarkably decreased the class A scavenger receptor and CD36 expression in the protein and mRNA levels. Astaxanthin also reduced MMP-1, -2, -3, -9, -12, and -14 activity and expression. The mRNA expression of tumor necrosis factor-α, interleukin-1β, interleukin-6, inducible nitric oxide synthase, and cyclooxygenase-2 were significantly suppressed by astaxanthin. Furthermore, astaxanthin inhibited the phosphorylation of nuclear factor-κB. Conclusions These results indicate that astaxanthin has inhibitory effects on macrophage activation, such as scavenger receptors up-regulation, MMPs activation, and pro-inflammatory cytokines secretion.</abstract><cop>Berlin/Heidelberg</cop><pub>Berlin/Heidelberg : Springer-Verlag</pub><pmid>19784539</pmid><doi>10.1007/s00394-009-0056-4</doi><tpages>8</tpages></addata></record> |
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| subjects | Antioxidants - pharmacology Atherosclerosis - prevention & control CD36 Antigens - genetics CD36 Antigens - metabolism Cell Line Chemistry Chemistry and Materials Science Cyclooxygenase 2 - genetics Cyclooxygenase 2 - metabolism Enzyme Activation - drug effects Gene Expression Regulation Humans Inflammation Mediators - metabolism Isoenzymes - genetics Isoenzymes - metabolism Macrophage Activation - drug effects Macrophages - drug effects Macrophages - metabolism Matrix Metalloproteinases - genetics Matrix Metalloproteinases - metabolism NF-kappa B - metabolism Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism Nutrition Original Contribution Phosphorylation Protein Processing, Post-Translational RNA, Messenger - metabolism Scavenger Receptors, Class A - genetics Scavenger Receptors, Class A - metabolism Xanthophylls - pharmacology |
| title | Astaxanthin suppresses scavenger receptor expression and matrix metalloproteinase activity in macrophages |
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