Isothiocyanates protect against oxidized LDL-induced endothelial dysfunction by upregulating Nrf2-dependent antioxidation and suppressing NFκB activation
Scope Oxidative stress plays a pivotal role in the pathophysiology of cardiovascular diseases. Oxidized low‐density lipoprotein (oxLDL) is a key contributor to atherogenesis through multiple mechanisms. In this study, we investigated the protection by three structurally related isothiocyanates, i.e....
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| Veröffentlicht in: | Molecular nutrition & food research 2013-11, Vol.57 (11), p.1918-1930 |
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| container_title | Molecular nutrition & food research |
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| creator | Huang, Chin-Shiu Lin, Ai-Hsuan Liu, Cheng-Tzu Tsai, Chia-Wen Chang, Ing-Shr Chen, Haw-Wen Lii, Chong-Kuei |
| description | Scope
Oxidative stress plays a pivotal role in the pathophysiology of cardiovascular diseases. Oxidized low‐density lipoprotein (oxLDL) is a key contributor to atherogenesis through multiple mechanisms. In this study, we investigated the protection by three structurally related isothiocyanates, i.e., sulforaphane (SFN), benzyl isothiocyanate (BITC), and phenethyl isocyanate (PEITC), against oxLDL‐induced leukocyte adhesion to vascular endothelium and the mechanism involved.
Methods and results
The protection against oxLDL‐induced endothelial dysfunction by isothiocyanates was studied in human umbilical vein endothelial cells (HUVECs). oxLDL increased reactive oxygen species (ROS) production, stimulated nuclear factor‐kappaB (NFκB) activation, and enhanced intercellular adhesion molecule 1 (ICAM‐1), vascular cell adhesion molecule 1 (VCAM‐1), and E‐selectin expression in HUVECs, which led to promotion of monocyte adhesion to HUVECs. Treatment with SFN, BITC, and PEITC (0–10 μM) dose‐dependently induced heme oxygenase (HO)‐1, glutamate cysteine ligase (GCL) catalytic and modifier subunit expression, intracellular glutathione content, and antioxidant response element (ARE)‐luciferase reporter activity. SFN, BITC, and PEITC pretreatment reversed oxLDL‐induced ROS production, NFκB nuclear translocation, κB‐reporter activity, ICAM‐1, VCAM‐1, and E‐selectin expression, and monocyte adhesion to endothelial cells. Both heme oxygenase 1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2) knockdown attenuated the isothiocyanate inhibition of oxLDL‐induced ROS production, κB‐reporter activity, and adhesion molecule expression.
Conclusion
SFN, BITC, and PEITC protect against oxLDL‐induced endothelial damage by upregulating Nrf2‐dependent HO‐1 and GCL expression, which leads to inhibition of NFκB activation and ICAM‐1, VCAM‐1, and E‐selectin expression. |
| doi_str_mv | 10.1002/mnfr.201300063 |
| format | Article |
| fullrecord | <record><control><sourceid>istex_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1002_mnfr_201300063</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>ark_67375_WNG_CSQRZ4TL_M</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4089-48ece05a92da688fc093531d8fe2f1b1d19612166afaca089bc3c9073809cd743</originalsourceid><addsrcrecordid>eNqF0MtuEzEYBWALgWgpbFkib1hO8GUuniWkpFSapmopQmJj_fElGCaekT0DHR6FR-lD9JlwkhKWrPwvvnMsHYReUjKjhLA3G2_DjBHKCSElf4SOaUl5llPOHx9uVhyhZzF-I4RTlvOn6IhxwctC1Mfo93nshq-uUxN4GEzEfegGowYMa3A-Dri7ddr9Mho3p03mvB5Vuo3XKWVaBy3WU7SjV4PrPF5NeOyDWY8tDM6v8TJYlmnTJ2986vRJpT7YYfAax7FPPsYdXtzfvcOQmn7swHP0xEIbzYuH9wR9Wry_mX_Imsuz8_nbJlM5EXWWC6MMKaBmGkohrCI1LzjVwhpm6YpqWpeU0bIECwpSYqW4qknFBamVrnJ-gmb7XhW6GIOxsg9uA2GSlMjtyHI7sjyMnAKv9oF-XG2MPvC_qybw-gFAVNDaAF65-M9VNc2pKJLL9-6na830n2_lxXJxzQjZ1mf7mIuDuT3EIHyXZcWrQn5ensn5x6vrL_lNIy_4H-l0qdI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Isothiocyanates protect against oxidized LDL-induced endothelial dysfunction by upregulating Nrf2-dependent antioxidation and suppressing NFκB activation</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Huang, Chin-Shiu ; Lin, Ai-Hsuan ; Liu, Cheng-Tzu ; Tsai, Chia-Wen ; Chang, Ing-Shr ; Chen, Haw-Wen ; Lii, Chong-Kuei</creator><creatorcontrib>Huang, Chin-Shiu ; Lin, Ai-Hsuan ; Liu, Cheng-Tzu ; Tsai, Chia-Wen ; Chang, Ing-Shr ; Chen, Haw-Wen ; Lii, Chong-Kuei</creatorcontrib><description>Scope
Oxidative stress plays a pivotal role in the pathophysiology of cardiovascular diseases. Oxidized low‐density lipoprotein (oxLDL) is a key contributor to atherogenesis through multiple mechanisms. In this study, we investigated the protection by three structurally related isothiocyanates, i.e., sulforaphane (SFN), benzyl isothiocyanate (BITC), and phenethyl isocyanate (PEITC), against oxLDL‐induced leukocyte adhesion to vascular endothelium and the mechanism involved.
Methods and results
The protection against oxLDL‐induced endothelial dysfunction by isothiocyanates was studied in human umbilical vein endothelial cells (HUVECs). oxLDL increased reactive oxygen species (ROS) production, stimulated nuclear factor‐kappaB (NFκB) activation, and enhanced intercellular adhesion molecule 1 (ICAM‐1), vascular cell adhesion molecule 1 (VCAM‐1), and E‐selectin expression in HUVECs, which led to promotion of monocyte adhesion to HUVECs. Treatment with SFN, BITC, and PEITC (0–10 μM) dose‐dependently induced heme oxygenase (HO)‐1, glutamate cysteine ligase (GCL) catalytic and modifier subunit expression, intracellular glutathione content, and antioxidant response element (ARE)‐luciferase reporter activity. SFN, BITC, and PEITC pretreatment reversed oxLDL‐induced ROS production, NFκB nuclear translocation, κB‐reporter activity, ICAM‐1, VCAM‐1, and E‐selectin expression, and monocyte adhesion to endothelial cells. Both heme oxygenase 1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2) knockdown attenuated the isothiocyanate inhibition of oxLDL‐induced ROS production, κB‐reporter activity, and adhesion molecule expression.
Conclusion
SFN, BITC, and PEITC protect against oxLDL‐induced endothelial damage by upregulating Nrf2‐dependent HO‐1 and GCL expression, which leads to inhibition of NFκB activation and ICAM‐1, VCAM‐1, and E‐selectin expression.</description><identifier>ISSN: 1613-4125</identifier><identifier>EISSN: 1613-4133</identifier><identifier>DOI: 10.1002/mnfr.201300063</identifier><identifier>PMID: 23836589</identifier><language>eng</language><publisher>Weinheim: Blackwell Publishing Ltd</publisher><subject>Adhesion molecules ; Antioxidant Response Elements - drug effects ; Antioxidants - pharmacology ; Biological and medical sciences ; Cell Adhesion - drug effects ; Dose-Response Relationship, Drug ; E-Selectin - genetics ; E-Selectin - metabolism ; Feeding. Feeding behavior ; Fundamental and applied biological sciences. Psychology ; Glutamate cysteine ligase ; Glutamate-Cysteine Ligase - genetics ; Glutamate-Cysteine Ligase - metabolism ; Heme oxygenase 1 ; Heme Oxygenase-1 - genetics ; Heme Oxygenase-1 - metabolism ; Human Umbilical Vein Endothelial Cells - drug effects ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Intercellular Adhesion Molecule-1 - genetics ; Intercellular Adhesion Molecule-1 - metabolism ; Isothiocyanates ; Isothiocyanates - pharmacology ; Leukocytes - drug effects ; Leukocytes - metabolism ; Lipoproteins, LDL - adverse effects ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; NF-kappa B - antagonists & inhibitors ; NF-kappa B - genetics ; NF-kappa B - metabolism ; Nuclear factor erythroid 2-related factor 2 (Nrf2) ; Nuclear factor-kappaB (NFκB) ; Oxidized LDL ; Reactive Oxygen Species - metabolism ; Up-Regulation ; Vascular Cell Adhesion Molecule-1 - genetics ; Vascular Cell Adhesion Molecule-1 - metabolism ; Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><ispartof>Molecular nutrition & food research, 2013-11, Vol.57 (11), p.1918-1930</ispartof><rights>2013 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><rights>2014 INIST-CNRS</rights><rights>2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4089-48ece05a92da688fc093531d8fe2f1b1d19612166afaca089bc3c9073809cd743</citedby><cites>FETCH-LOGICAL-c4089-48ece05a92da688fc093531d8fe2f1b1d19612166afaca089bc3c9073809cd743</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.201300063$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fmnfr.201300063$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27914185$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23836589$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Chin-Shiu</creatorcontrib><creatorcontrib>Lin, Ai-Hsuan</creatorcontrib><creatorcontrib>Liu, Cheng-Tzu</creatorcontrib><creatorcontrib>Tsai, Chia-Wen</creatorcontrib><creatorcontrib>Chang, Ing-Shr</creatorcontrib><creatorcontrib>Chen, Haw-Wen</creatorcontrib><creatorcontrib>Lii, Chong-Kuei</creatorcontrib><title>Isothiocyanates protect against oxidized LDL-induced endothelial dysfunction by upregulating Nrf2-dependent antioxidation and suppressing NFκB activation</title><title>Molecular nutrition & food research</title><addtitle>Mol. Nutr. Food Res</addtitle><description>Scope
Oxidative stress plays a pivotal role in the pathophysiology of cardiovascular diseases. Oxidized low‐density lipoprotein (oxLDL) is a key contributor to atherogenesis through multiple mechanisms. In this study, we investigated the protection by three structurally related isothiocyanates, i.e., sulforaphane (SFN), benzyl isothiocyanate (BITC), and phenethyl isocyanate (PEITC), against oxLDL‐induced leukocyte adhesion to vascular endothelium and the mechanism involved.
Methods and results
The protection against oxLDL‐induced endothelial dysfunction by isothiocyanates was studied in human umbilical vein endothelial cells (HUVECs). oxLDL increased reactive oxygen species (ROS) production, stimulated nuclear factor‐kappaB (NFκB) activation, and enhanced intercellular adhesion molecule 1 (ICAM‐1), vascular cell adhesion molecule 1 (VCAM‐1), and E‐selectin expression in HUVECs, which led to promotion of monocyte adhesion to HUVECs. Treatment with SFN, BITC, and PEITC (0–10 μM) dose‐dependently induced heme oxygenase (HO)‐1, glutamate cysteine ligase (GCL) catalytic and modifier subunit expression, intracellular glutathione content, and antioxidant response element (ARE)‐luciferase reporter activity. SFN, BITC, and PEITC pretreatment reversed oxLDL‐induced ROS production, NFκB nuclear translocation, κB‐reporter activity, ICAM‐1, VCAM‐1, and E‐selectin expression, and monocyte adhesion to endothelial cells. Both heme oxygenase 1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2) knockdown attenuated the isothiocyanate inhibition of oxLDL‐induced ROS production, κB‐reporter activity, and adhesion molecule expression.
Conclusion
SFN, BITC, and PEITC protect against oxLDL‐induced endothelial damage by upregulating Nrf2‐dependent HO‐1 and GCL expression, which leads to inhibition of NFκB activation and ICAM‐1, VCAM‐1, and E‐selectin expression.</description><subject>Adhesion molecules</subject><subject>Antioxidant Response Elements - drug effects</subject><subject>Antioxidants - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Adhesion - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>E-Selectin - genetics</subject><subject>E-Selectin - metabolism</subject><subject>Feeding. Feeding behavior</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glutamate cysteine ligase</subject><subject>Glutamate-Cysteine Ligase - genetics</subject><subject>Glutamate-Cysteine Ligase - metabolism</subject><subject>Heme oxygenase 1</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Isothiocyanates</subject><subject>Isothiocyanates - pharmacology</subject><subject>Leukocytes - drug effects</subject><subject>Leukocytes - metabolism</subject><subject>Lipoproteins, LDL - adverse effects</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-kappa B - genetics</subject><subject>NF-kappa B - metabolism</subject><subject>Nuclear factor erythroid 2-related factor 2 (Nrf2)</subject><subject>Nuclear factor-kappaB (NFκB)</subject><subject>Oxidized LDL</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Up-Regulation</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><subject>Vertebrates: anatomy and physiology, studies on body, several organs or systems</subject><issn>1613-4125</issn><issn>1613-4133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0MtuEzEYBWALgWgpbFkib1hO8GUuniWkpFSapmopQmJj_fElGCaekT0DHR6FR-lD9JlwkhKWrPwvvnMsHYReUjKjhLA3G2_DjBHKCSElf4SOaUl5llPOHx9uVhyhZzF-I4RTlvOn6IhxwctC1Mfo93nshq-uUxN4GEzEfegGowYMa3A-Dri7ddr9Mho3p03mvB5Vuo3XKWVaBy3WU7SjV4PrPF5NeOyDWY8tDM6v8TJYlmnTJ2986vRJpT7YYfAax7FPPsYdXtzfvcOQmn7swHP0xEIbzYuH9wR9Wry_mX_Imsuz8_nbJlM5EXWWC6MMKaBmGkohrCI1LzjVwhpm6YpqWpeU0bIECwpSYqW4qknFBamVrnJ-gmb7XhW6GIOxsg9uA2GSlMjtyHI7sjyMnAKv9oF-XG2MPvC_qybw-gFAVNDaAF65-M9VNc2pKJLL9-6na830n2_lxXJxzQjZ1mf7mIuDuT3EIHyXZcWrQn5ensn5x6vrL_lNIy_4H-l0qdI</recordid><startdate>201311</startdate><enddate>201311</enddate><creator>Huang, Chin-Shiu</creator><creator>Lin, Ai-Hsuan</creator><creator>Liu, Cheng-Tzu</creator><creator>Tsai, Chia-Wen</creator><creator>Chang, Ing-Shr</creator><creator>Chen, Haw-Wen</creator><creator>Lii, Chong-Kuei</creator><general>Blackwell Publishing 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></search><sort><creationdate>201311</creationdate><title>Isothiocyanates protect against oxidized LDL-induced endothelial dysfunction by upregulating Nrf2-dependent antioxidation and suppressing NFκB activation</title><author>Huang, Chin-Shiu ; Lin, Ai-Hsuan ; Liu, Cheng-Tzu ; Tsai, Chia-Wen ; Chang, Ing-Shr ; Chen, Haw-Wen ; Lii, Chong-Kuei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4089-48ece05a92da688fc093531d8fe2f1b1d19612166afaca089bc3c9073809cd743</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adhesion molecules</topic><topic>Antioxidant Response Elements - drug effects</topic><topic>Antioxidants - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Adhesion - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>E-Selectin - genetics</topic><topic>E-Selectin - metabolism</topic><topic>Feeding. Feeding behavior</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glutamate cysteine ligase</topic><topic>Glutamate-Cysteine Ligase - genetics</topic><topic>Glutamate-Cysteine Ligase - metabolism</topic><topic>Heme oxygenase 1</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Human Umbilical Vein Endothelial Cells - drug effects</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Isothiocyanates</topic><topic>Isothiocyanates - pharmacology</topic><topic>Leukocytes - drug effects</topic><topic>Leukocytes - metabolism</topic><topic>Lipoproteins, LDL - adverse effects</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-kappa B - genetics</topic><topic>NF-kappa B - metabolism</topic><topic>Nuclear factor erythroid 2-related factor 2 (Nrf2)</topic><topic>Nuclear factor-kappaB (NFκB)</topic><topic>Oxidized LDL</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Up-Regulation</topic><topic>Vascular Cell Adhesion Molecule-1 - genetics</topic><topic>Vascular Cell Adhesion Molecule-1 - metabolism</topic><topic>Vertebrates: anatomy and physiology, studies on body, several organs or systems</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Chin-Shiu</creatorcontrib><creatorcontrib>Lin, Ai-Hsuan</creatorcontrib><creatorcontrib>Liu, Cheng-Tzu</creatorcontrib><creatorcontrib>Tsai, Chia-Wen</creatorcontrib><creatorcontrib>Chang, Ing-Shr</creatorcontrib><creatorcontrib>Chen, Haw-Wen</creatorcontrib><creatorcontrib>Lii, Chong-Kuei</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><jtitle>Molecular nutrition & food research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Chin-Shiu</au><au>Lin, Ai-Hsuan</au><au>Liu, Cheng-Tzu</au><au>Tsai, Chia-Wen</au><au>Chang, Ing-Shr</au><au>Chen, Haw-Wen</au><au>Lii, Chong-Kuei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isothiocyanates protect against oxidized LDL-induced endothelial dysfunction by upregulating Nrf2-dependent antioxidation and suppressing NFκB activation</atitle><jtitle>Molecular nutrition & food research</jtitle><addtitle>Mol. Nutr. Food Res</addtitle><date>2013-11</date><risdate>2013</risdate><volume>57</volume><issue>11</issue><spage>1918</spage><epage>1930</epage><pages>1918-1930</pages><issn>1613-4125</issn><eissn>1613-4133</eissn><abstract>Scope
Oxidative stress plays a pivotal role in the pathophysiology of cardiovascular diseases. Oxidized low‐density lipoprotein (oxLDL) is a key contributor to atherogenesis through multiple mechanisms. In this study, we investigated the protection by three structurally related isothiocyanates, i.e., sulforaphane (SFN), benzyl isothiocyanate (BITC), and phenethyl isocyanate (PEITC), against oxLDL‐induced leukocyte adhesion to vascular endothelium and the mechanism involved.
Methods and results
The protection against oxLDL‐induced endothelial dysfunction by isothiocyanates was studied in human umbilical vein endothelial cells (HUVECs). oxLDL increased reactive oxygen species (ROS) production, stimulated nuclear factor‐kappaB (NFκB) activation, and enhanced intercellular adhesion molecule 1 (ICAM‐1), vascular cell adhesion molecule 1 (VCAM‐1), and E‐selectin expression in HUVECs, which led to promotion of monocyte adhesion to HUVECs. Treatment with SFN, BITC, and PEITC (0–10 μM) dose‐dependently induced heme oxygenase (HO)‐1, glutamate cysteine ligase (GCL) catalytic and modifier subunit expression, intracellular glutathione content, and antioxidant response element (ARE)‐luciferase reporter activity. SFN, BITC, and PEITC pretreatment reversed oxLDL‐induced ROS production, NFκB nuclear translocation, κB‐reporter activity, ICAM‐1, VCAM‐1, and E‐selectin expression, and monocyte adhesion to endothelial cells. Both heme oxygenase 1 (HO‐1) and nuclear factor erythroid 2‐related factor 2 (Nrf2) knockdown attenuated the isothiocyanate inhibition of oxLDL‐induced ROS production, κB‐reporter activity, and adhesion molecule expression.
Conclusion
SFN, BITC, and PEITC protect against oxLDL‐induced endothelial damage by upregulating Nrf2‐dependent HO‐1 and GCL expression, which leads to inhibition of NFκB activation and ICAM‐1, VCAM‐1, and E‐selectin expression.</abstract><cop>Weinheim</cop><pub>Blackwell Publishing Ltd</pub><pmid>23836589</pmid><doi>10.1002/mnfr.201300063</doi><tpages>13</tpages></addata></record> |
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| ispartof | Molecular nutrition & food research, 2013-11, Vol.57 (11), p.1918-1930 |
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| subjects | Adhesion molecules Antioxidant Response Elements - drug effects Antioxidants - pharmacology Biological and medical sciences Cell Adhesion - drug effects Dose-Response Relationship, Drug E-Selectin - genetics E-Selectin - metabolism Feeding. Feeding behavior Fundamental and applied biological sciences. Psychology Glutamate cysteine ligase Glutamate-Cysteine Ligase - genetics Glutamate-Cysteine Ligase - metabolism Heme oxygenase 1 Heme Oxygenase-1 - genetics Heme Oxygenase-1 - metabolism Human Umbilical Vein Endothelial Cells - drug effects Human Umbilical Vein Endothelial Cells - metabolism Humans Intercellular Adhesion Molecule-1 - genetics Intercellular Adhesion Molecule-1 - metabolism Isothiocyanates Isothiocyanates - pharmacology Leukocytes - drug effects Leukocytes - metabolism Lipoproteins, LDL - adverse effects NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism NF-kappa B - antagonists & inhibitors NF-kappa B - genetics NF-kappa B - metabolism Nuclear factor erythroid 2-related factor 2 (Nrf2) Nuclear factor-kappaB (NFκB) Oxidized LDL Reactive Oxygen Species - metabolism Up-Regulation Vascular Cell Adhesion Molecule-1 - genetics Vascular Cell Adhesion Molecule-1 - metabolism Vertebrates: anatomy and physiology, studies on body, several organs or systems |
| title | Isothiocyanates protect against oxidized LDL-induced endothelial dysfunction by upregulating Nrf2-dependent antioxidation and suppressing NFκB activation |
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