Diallyl disulfide and diallyl trisulfide protect endothelial nitric oxide synthase against damage by oxidized low-density lipoprotein
Garlic is viewed as an effective health food against atherosclerosis. In this study, we examined whether diallyl disulfide (DADS) and diallyl trisulfide (DATS) protect endothelial nitric oxide synthase (eNOS) activation against oxidized LDL (ox-LDL) insult and through what mechanism. We found that D...
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| Veröffentlicht in: | Molecular nutrition & food research 2010-05, Vol.54 (S1), p.S42-S52 |
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| creator | Lei, Yen-Ping Liu, Cheng-Tzu Sheen, Lee-Yan Chen, Haw-Wen Lii, Chong-Kuei |
| description | Garlic is viewed as an effective health food against atherosclerosis. In this study, we examined whether diallyl disulfide (DADS) and diallyl trisulfide (DATS) protect endothelial nitric oxide synthase (eNOS) activation against oxidized LDL (ox-LDL) insult and through what mechanism. We found that DADS and DATS reversed the suppression of eNOS Ser1177 phosphorylation by ox-LDL, and wortmannin abolished the reversal by DADS and DATS. Similarly, the inhibition of cellular cGMP and nitric oxide production by ox-LDL was reversed by DADS and DATS (p |
| doi_str_mv | 10.1002/mnfr.200900278 |
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In this study, we examined whether diallyl disulfide (DADS) and diallyl trisulfide (DATS) protect endothelial nitric oxide synthase (eNOS) activation against oxidized LDL (ox-LDL) insult and through what mechanism. We found that DADS and DATS reversed the suppression of eNOS Ser1177 phosphorylation by ox-LDL, and wortmannin abolished the reversal by DADS and DATS. Similarly, the inhibition of cellular cGMP and nitric oxide production by ox-LDL was reversed by DADS and DATS (p<0.05). This increase in nitric oxide bioavailability by the allyl sulfides was attenuated by wortmannin. Immunoprecipitation assay revealed that DADS and DATS preserved the interaction of eNOS with caveolin-1 in the membrane. In addition, DADS and DATS suppressed the reduction of the cellular eNOS protein content by ox-LDL. When cycloheximide was added to block protein synthesis, DADS and DATS suppressed eNOS protein degradation similarly to that noted by MG132. Ox-LDL increased chymotrypsin-like proteasome activity, and this increase was inhibited by the allyl sulfides and MG132 (p<0.05). These results suggest that DADS and DATS protect eNOS activity against ox-LDL insult. This protection can be attributed partly to their mediation of phosphatidylinositol 3-kinase/protein kinase B signaling and prevention of eNOS degradation.</description><identifier>ISSN: 1613-4125</identifier><identifier>EISSN: 1613-4133</identifier><identifier>DOI: 10.1002/mnfr.200900278</identifier><identifier>PMID: 20229525</identifier><language>eng</language><publisher>Weinheim: Wiley-VCH Verlag</publisher><subject>Allyl Compounds - pharmacology ; Caveolin 1 - drug effects ; Caveolin 1 - metabolism ; Cyclic GMP - metabolism ; Diallyl disulfide ; Diallyl trisulfide ; Disulfides - pharmacology ; DNA Primers ; Endothelial nitric oxide synthase ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Garlic ; Humans ; Lipoproteins, LDL - blood ; Lipoproteins, LDL - pharmacology ; Nitric Oxide Synthase Type III - drug effects ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; Proteasome ; Proteasome Endopeptidase Complex - metabolism ; Protein kinase B ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; Sulfides - pharmacology ; Umbilical Veins - physiology</subject><ispartof>Molecular nutrition & food research, 2010-05, Vol.54 (S1), p.S42-S52</ispartof><rights>Copyright © 2010 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4028-8d68cabd6facd7a6b64c9178c673773011b923bb087d23402443185a0129d6753</citedby><cites>FETCH-LOGICAL-c4028-8d68cabd6facd7a6b64c9178c673773011b923bb087d23402443185a0129d6753</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%2Fmnfr.200900278$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmnfr.200900278$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20229525$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lei, Yen-Ping</creatorcontrib><creatorcontrib>Liu, Cheng-Tzu</creatorcontrib><creatorcontrib>Sheen, Lee-Yan</creatorcontrib><creatorcontrib>Chen, Haw-Wen</creatorcontrib><creatorcontrib>Lii, Chong-Kuei</creatorcontrib><title>Diallyl disulfide and diallyl trisulfide protect endothelial nitric oxide synthase against damage by oxidized low-density lipoprotein</title><title>Molecular nutrition & food research</title><addtitle>Mol. Nutr. Food Res</addtitle><description>Garlic is viewed as an effective health food against atherosclerosis. In this study, we examined whether diallyl disulfide (DADS) and diallyl trisulfide (DATS) protect endothelial nitric oxide synthase (eNOS) activation against oxidized LDL (ox-LDL) insult and through what mechanism. We found that DADS and DATS reversed the suppression of eNOS Ser1177 phosphorylation by ox-LDL, and wortmannin abolished the reversal by DADS and DATS. Similarly, the inhibition of cellular cGMP and nitric oxide production by ox-LDL was reversed by DADS and DATS (p<0.05). This increase in nitric oxide bioavailability by the allyl sulfides was attenuated by wortmannin. Immunoprecipitation assay revealed that DADS and DATS preserved the interaction of eNOS with caveolin-1 in the membrane. In addition, DADS and DATS suppressed the reduction of the cellular eNOS protein content by ox-LDL. When cycloheximide was added to block protein synthesis, DADS and DATS suppressed eNOS protein degradation similarly to that noted by MG132. Ox-LDL increased chymotrypsin-like proteasome activity, and this increase was inhibited by the allyl sulfides and MG132 (p<0.05). These results suggest that DADS and DATS protect eNOS activity against ox-LDL insult. This protection can be attributed partly to their mediation of phosphatidylinositol 3-kinase/protein kinase B signaling and prevention of eNOS degradation.</description><subject>Allyl Compounds - pharmacology</subject><subject>Caveolin 1 - drug effects</subject><subject>Caveolin 1 - metabolism</subject><subject>Cyclic GMP - metabolism</subject><subject>Diallyl disulfide</subject><subject>Diallyl trisulfide</subject><subject>Disulfides - pharmacology</subject><subject>DNA Primers</subject><subject>Endothelial nitric oxide synthase</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - physiology</subject><subject>Garlic</subject><subject>Humans</subject><subject>Lipoproteins, LDL - blood</subject><subject>Lipoproteins, LDL - pharmacology</subject><subject>Nitric Oxide Synthase Type III - drug effects</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Proteasome</subject><subject>Proteasome Endopeptidase Complex - metabolism</subject><subject>Protein kinase B</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>Sulfides - pharmacology</subject><subject>Umbilical Veins - physiology</subject><issn>1613-4125</issn><issn>1613-4133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtP3DAURq0KxGNg22XrHasMfiRxskTQmRbBVCog2FmO7QxuHWcaewTpvv8bzwQidqx879W5x_JnAD5jNMUIkdPG1d2UIFTGhhWfwAHOMU1STOnOWJNsHxx6_xshiklK98A-QYSUGckOwP8LI6ztLVTGr21tlIbCqdgN09CN41XXBi0D1E614VHbSEBnIiBh-7wBfO_Co_BRsBTG-QCVaMRSw6rfAuafVtC2T4nSzpvQQ2tW7VZq3BHYrYX1-vj1nIC72bfb8-_J1c_5j_Ozq0SmiBRJofJCikrltZCKibzKU1liVsicUcYowrgqCa0qVDBFaFxJU4qLTCBMSpWzjE7AyeCN9_5dax94Y7zU1gqn27XnjNIsIzi6JmA6kLJrve90zVedaUTXc4z4Jnm-SZ6PyceFL6_qddVoNeJvUUegHIAnY3X_gY5fL2a_3suTYdf4oJ_HXdH94ZunZ_x-MecPD7MbfHvJ-DzyXwe-Fi0Xy_iJ_O6GIBwjKlKSxuIF-nSq9g</recordid><startdate>201005</startdate><enddate>201005</enddate><creator>Lei, Yen-Ping</creator><creator>Liu, Cheng-Tzu</creator><creator>Sheen, Lee-Yan</creator><creator>Chen, Haw-Wen</creator><creator>Lii, Chong-Kuei</creator><general>Wiley-VCH Verlag</general><general>WILEY-VCH Verlag</general><general>WILEY‐VCH Verlag</general><scope>FBQ</scope><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>7X8</scope></search><sort><creationdate>201005</creationdate><title>Diallyl disulfide and diallyl trisulfide protect endothelial nitric oxide synthase against damage by oxidized low-density lipoprotein</title><author>Lei, Yen-Ping ; Liu, Cheng-Tzu ; Sheen, Lee-Yan ; Chen, Haw-Wen ; Lii, Chong-Kuei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4028-8d68cabd6facd7a6b64c9178c673773011b923bb087d23402443185a0129d6753</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Allyl Compounds - pharmacology</topic><topic>Caveolin 1 - drug effects</topic><topic>Caveolin 1 - metabolism</topic><topic>Cyclic GMP - metabolism</topic><topic>Diallyl disulfide</topic><topic>Diallyl trisulfide</topic><topic>Disulfides - pharmacology</topic><topic>DNA Primers</topic><topic>Endothelial nitric oxide synthase</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - physiology</topic><topic>Garlic</topic><topic>Humans</topic><topic>Lipoproteins, LDL - blood</topic><topic>Lipoproteins, LDL - pharmacology</topic><topic>Nitric Oxide Synthase Type III - drug effects</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Proteasome</topic><topic>Proteasome Endopeptidase Complex - metabolism</topic><topic>Protein kinase B</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>Sulfides - pharmacology</topic><topic>Umbilical Veins - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lei, Yen-Ping</creatorcontrib><creatorcontrib>Liu, Cheng-Tzu</creatorcontrib><creatorcontrib>Sheen, Lee-Yan</creatorcontrib><creatorcontrib>Chen, Haw-Wen</creatorcontrib><creatorcontrib>Lii, Chong-Kuei</creatorcontrib><collection>AGRIS</collection><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>MEDLINE - Academic</collection><jtitle>Molecular nutrition & food research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lei, Yen-Ping</au><au>Liu, Cheng-Tzu</au><au>Sheen, Lee-Yan</au><au>Chen, Haw-Wen</au><au>Lii, Chong-Kuei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Diallyl disulfide and diallyl trisulfide protect endothelial nitric oxide synthase against damage by oxidized low-density lipoprotein</atitle><jtitle>Molecular nutrition & food research</jtitle><addtitle>Mol. Nutr. Food Res</addtitle><date>2010-05</date><risdate>2010</risdate><volume>54</volume><issue>S1</issue><spage>S42</spage><epage>S52</epage><pages>S42-S52</pages><issn>1613-4125</issn><eissn>1613-4133</eissn><abstract>Garlic is viewed as an effective health food against atherosclerosis. In this study, we examined whether diallyl disulfide (DADS) and diallyl trisulfide (DATS) protect endothelial nitric oxide synthase (eNOS) activation against oxidized LDL (ox-LDL) insult and through what mechanism. We found that DADS and DATS reversed the suppression of eNOS Ser1177 phosphorylation by ox-LDL, and wortmannin abolished the reversal by DADS and DATS. Similarly, the inhibition of cellular cGMP and nitric oxide production by ox-LDL was reversed by DADS and DATS (p<0.05). This increase in nitric oxide bioavailability by the allyl sulfides was attenuated by wortmannin. Immunoprecipitation assay revealed that DADS and DATS preserved the interaction of eNOS with caveolin-1 in the membrane. In addition, DADS and DATS suppressed the reduction of the cellular eNOS protein content by ox-LDL. When cycloheximide was added to block protein synthesis, DADS and DATS suppressed eNOS protein degradation similarly to that noted by MG132. Ox-LDL increased chymotrypsin-like proteasome activity, and this increase was inhibited by the allyl sulfides and MG132 (p<0.05). These results suggest that DADS and DATS protect eNOS activity against ox-LDL insult. This protection can be attributed partly to their mediation of phosphatidylinositol 3-kinase/protein kinase B signaling and prevention of eNOS degradation.</abstract><cop>Weinheim</cop><pub>Wiley-VCH Verlag</pub><pmid>20229525</pmid><doi>10.1002/mnfr.200900278</doi><tpages>11</tpages></addata></record> |
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| subjects | Allyl Compounds - pharmacology Caveolin 1 - drug effects Caveolin 1 - metabolism Cyclic GMP - metabolism Diallyl disulfide Diallyl trisulfide Disulfides - pharmacology DNA Primers Endothelial nitric oxide synthase Endothelium, Vascular - drug effects Endothelium, Vascular - physiology Garlic Humans Lipoproteins, LDL - blood Lipoproteins, LDL - pharmacology Nitric Oxide Synthase Type III - drug effects Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - metabolism Proteasome Proteasome Endopeptidase Complex - metabolism Protein kinase B Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics Sulfides - pharmacology Umbilical Veins - physiology |
| title | Diallyl disulfide and diallyl trisulfide protect endothelial nitric oxide synthase against damage by oxidized low-density lipoprotein |
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