Tyrosol Attenuates Ischemia–Reperfusion-Induced Kidney Injury via Inhibition of Inducible Nitric Oxide Synthase
Tyrosol is a natural phenolic antioxidant compound. Oxidative stress represents one of the important mechanisms underlying ischemia–reperfusion-induced kidney injury. The aim of this study was to investigate the effect of tyrosol against ischemia–reperfusion-induced acute kidney injury. The left kid...
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| Veröffentlicht in: | Journal of agricultural and food chemistry 2013-04, Vol.61 (15), p.3669-3675 |
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| creator | Wang, Pengqi Zhu, Qingjun Wu, Nan Siow, Yaw L Aukema, Harold O, Karmin |
| description | Tyrosol is a natural phenolic antioxidant compound. Oxidative stress represents one of the important mechanisms underlying ischemia–reperfusion-induced kidney injury. The aim of this study was to investigate the effect of tyrosol against ischemia–reperfusion-induced acute kidney injury. The left kidney of Sprague–Dawley rats was subjected to 45 min of ischemia followed by reperfusion for 6 h. Ischemia–reperfusion caused an increase in peroxynitrite formation and lipid peroxidation. The level of nitric oxide (NO) metabolites and the mRNA of inducible nitric oxide synthase (iNOS) were elevated in ischemia-reperfused kidneys. Administration of tyrosol (100 mg/kg body weight) to rats prior to the induction of ischemia significantly reduced peroxynitrite formation, lipid peroxidation, and the level of NO metabolites. Tyrosol administration also attenuated ischemia–reperfusion-induced NF-κB activation and iNOS expression. Such a treatment improved kidney function. Results suggest that tyrosol may have a protective effect against acute kidney injury through inhibition of iNOS-mediated oxidative stress. |
| doi_str_mv | 10.1021/jf400227u |
| format | Article |
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Oxidative stress represents one of the important mechanisms underlying ischemia–reperfusion-induced kidney injury. The aim of this study was to investigate the effect of tyrosol against ischemia–reperfusion-induced acute kidney injury. The left kidney of Sprague–Dawley rats was subjected to 45 min of ischemia followed by reperfusion for 6 h. Ischemia–reperfusion caused an increase in peroxynitrite formation and lipid peroxidation. The level of nitric oxide (NO) metabolites and the mRNA of inducible nitric oxide synthase (iNOS) were elevated in ischemia-reperfused kidneys. Administration of tyrosol (100 mg/kg body weight) to rats prior to the induction of ischemia significantly reduced peroxynitrite formation, lipid peroxidation, and the level of NO metabolites. Tyrosol administration also attenuated ischemia–reperfusion-induced NF-κB activation and iNOS expression. Such a treatment improved kidney function. Results suggest that tyrosol may have a protective effect against acute kidney injury through inhibition of iNOS-mediated oxidative stress.</description><identifier>ISSN: 0021-8561</identifier><identifier>EISSN: 1520-5118</identifier><identifier>DOI: 10.1021/jf400227u</identifier><identifier>PMID: 23566115</identifier><identifier>CODEN: JAFCAU</identifier><language>eng</language><publisher>Washington, DC: American Chemical Society</publisher><subject>Animals ; Antioxidants - administration & dosage ; Antioxidants - therapeutic use ; Biological and medical sciences ; body weight ; Dose-Response Relationship, Drug ; Down-Regulation - drug effects ; Food industries ; Fundamental and applied biological sciences. Psychology ; Injections, Intraperitoneal ; ischemia ; Kidney - blood supply ; Kidney - drug effects ; Kidney - metabolism ; Kidney - physiopathology ; kidneys ; lipid peroxidation ; Lipid Peroxidation - drug effects ; Male ; messenger RNA ; metabolites ; nitric oxide ; Nitric Oxide - metabolism ; nitric oxide synthase ; Nitric Oxide Synthase Type II - genetics ; Nitric Oxide Synthase Type II - metabolism ; oxidative stress ; Oxidative Stress - drug effects ; Phenylethyl Alcohol - administration & dosage ; Phenylethyl Alcohol - analogs & derivatives ; Phenylethyl Alcohol - therapeutic use ; protective effect ; Rats ; Rats, Sprague-Dawley ; renal function ; Reperfusion Injury - metabolism ; Reperfusion Injury - physiopathology ; Reperfusion Injury - prevention & control ; RNA, Messenger - metabolism</subject><ispartof>Journal of agricultural and food chemistry, 2013-04, Vol.61 (15), p.3669-3675</ispartof><rights>Copyright © 2013 American Chemical Society</rights><rights>2014 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a369t-4abe5c1b6a3951d63fc60c825f9fff82208d51905f643cff336fec2fa8b0271c3</citedby><cites>FETCH-LOGICAL-a369t-4abe5c1b6a3951d63fc60c825f9fff82208d51905f643cff336fec2fa8b0271c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://pubs.acs.org/doi/pdf/10.1021/jf400227u$$EPDF$$P50$$Gacs$$H</linktopdf><linktohtml>$$Uhttps://pubs.acs.org/doi/10.1021/jf400227u$$EHTML$$P50$$Gacs$$H</linktohtml><link.rule.ids>314,780,784,2763,27075,27923,27924,56737,56787</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27282953$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23566115$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Pengqi</creatorcontrib><creatorcontrib>Zhu, Qingjun</creatorcontrib><creatorcontrib>Wu, Nan</creatorcontrib><creatorcontrib>Siow, Yaw L</creatorcontrib><creatorcontrib>Aukema, Harold</creatorcontrib><creatorcontrib>O, Karmin</creatorcontrib><title>Tyrosol Attenuates Ischemia–Reperfusion-Induced Kidney Injury via Inhibition of Inducible Nitric Oxide Synthase</title><title>Journal of agricultural and food chemistry</title><addtitle>J. Agric. Food Chem</addtitle><description>Tyrosol is a natural phenolic antioxidant compound. Oxidative stress represents one of the important mechanisms underlying ischemia–reperfusion-induced kidney injury. The aim of this study was to investigate the effect of tyrosol against ischemia–reperfusion-induced acute kidney injury. The left kidney of Sprague–Dawley rats was subjected to 45 min of ischemia followed by reperfusion for 6 h. Ischemia–reperfusion caused an increase in peroxynitrite formation and lipid peroxidation. The level of nitric oxide (NO) metabolites and the mRNA of inducible nitric oxide synthase (iNOS) were elevated in ischemia-reperfused kidneys. Administration of tyrosol (100 mg/kg body weight) to rats prior to the induction of ischemia significantly reduced peroxynitrite formation, lipid peroxidation, and the level of NO metabolites. Tyrosol administration also attenuated ischemia–reperfusion-induced NF-κB activation and iNOS expression. Such a treatment improved kidney function. Results suggest that tyrosol may have a protective effect against acute kidney injury through inhibition of iNOS-mediated oxidative stress.</description><subject>Animals</subject><subject>Antioxidants - administration & dosage</subject><subject>Antioxidants - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>body weight</subject><subject>Dose-Response Relationship, Drug</subject><subject>Down-Regulation - drug effects</subject><subject>Food industries</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Injections, Intraperitoneal</subject><subject>ischemia</subject><subject>Kidney - blood supply</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - physiopathology</subject><subject>kidneys</subject><subject>lipid peroxidation</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>messenger RNA</subject><subject>metabolites</subject><subject>nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>nitric oxide synthase</subject><subject>Nitric Oxide Synthase Type II - genetics</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Phenylethyl Alcohol - administration & dosage</subject><subject>Phenylethyl Alcohol - analogs & derivatives</subject><subject>Phenylethyl Alcohol - therapeutic use</subject><subject>protective effect</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>renal function</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - physiopathology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>RNA, Messenger - metabolism</subject><issn>0021-8561</issn><issn>1520-5118</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpt0MFu1DAQBmALgehSOPAC4EslOAQ89tpxjlVVYEVFJdqeI8cZs15lna0dI3LrO_CGPAmGXQoHTh5Zn_4Z_YQ8B_YGGIe3G7dkjPM6PyALkJxVEkA_JIvyCZWWCo7Ik5Q2jDEta_aYHHEhlQKQC3J7PccxjQM9nSYM2UyY6CrZNW69-XH3_TPuMLqc_BiqVeizxZ5-9H3Ama7CJseZfvWmjGvf-akgOjr62_luQPrJT9FbevnN90iv5jCtTcKn5JEzQ8Jnh_eY3Lw7vz77UF1cvl-dnV5URqhmqpamQ2mhU0Y0EnolnFXMai5d45zTnDPdS2iYdGoprHNCKIeWO6M7xmuw4pi82ufu4nibMU3t1ieLw2ACjjm1IAQwXYsGCn29p7Z0kSK6dhf91sS5Bdb-ari9b7jYF4fY3G2xv5d_Ki3g5ABMsmZw0QTr019Xc80bKYp7uXfOjK35Eou5ueIMyiIQjOt_koxN7WbMMZS-_nPST1W3mnE</recordid><startdate>20130417</startdate><enddate>20130417</enddate><creator>Wang, Pengqi</creator><creator>Zhu, Qingjun</creator><creator>Wu, Nan</creator><creator>Siow, Yaw L</creator><creator>Aukema, Harold</creator><creator>O, Karmin</creator><general>American Chemical Society</general><scope>FBQ</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><scope>7X8</scope></search><sort><creationdate>20130417</creationdate><title>Tyrosol Attenuates Ischemia–Reperfusion-Induced Kidney Injury via Inhibition of Inducible Nitric Oxide Synthase</title><author>Wang, Pengqi ; Zhu, Qingjun ; Wu, Nan ; Siow, Yaw L ; Aukema, Harold ; O, Karmin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a369t-4abe5c1b6a3951d63fc60c825f9fff82208d51905f643cff336fec2fa8b0271c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Antioxidants - administration & dosage</topic><topic>Antioxidants - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>body weight</topic><topic>Dose-Response Relationship, Drug</topic><topic>Down-Regulation - drug effects</topic><topic>Food industries</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Injections, Intraperitoneal</topic><topic>ischemia</topic><topic>Kidney - blood supply</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - physiopathology</topic><topic>kidneys</topic><topic>lipid peroxidation</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>messenger RNA</topic><topic>metabolites</topic><topic>nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>nitric oxide synthase</topic><topic>Nitric Oxide Synthase Type II - genetics</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Phenylethyl Alcohol - administration & dosage</topic><topic>Phenylethyl Alcohol - analogs & derivatives</topic><topic>Phenylethyl Alcohol - therapeutic use</topic><topic>protective effect</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>renal function</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - physiopathology</topic><topic>Reperfusion Injury - prevention & control</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Pengqi</creatorcontrib><creatorcontrib>Zhu, Qingjun</creatorcontrib><creatorcontrib>Wu, Nan</creatorcontrib><creatorcontrib>Siow, Yaw L</creatorcontrib><creatorcontrib>Aukema, Harold</creatorcontrib><creatorcontrib>O, Karmin</creatorcontrib><collection>AGRIS</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><collection>MEDLINE - Academic</collection><jtitle>Journal of agricultural and food chemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Pengqi</au><au>Zhu, Qingjun</au><au>Wu, Nan</au><au>Siow, Yaw L</au><au>Aukema, Harold</au><au>O, Karmin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tyrosol Attenuates Ischemia–Reperfusion-Induced Kidney Injury via Inhibition of Inducible Nitric Oxide Synthase</atitle><jtitle>Journal of agricultural and food chemistry</jtitle><addtitle>J. Agric. Food Chem</addtitle><date>2013-04-17</date><risdate>2013</risdate><volume>61</volume><issue>15</issue><spage>3669</spage><epage>3675</epage><pages>3669-3675</pages><issn>0021-8561</issn><eissn>1520-5118</eissn><coden>JAFCAU</coden><abstract>Tyrosol is a natural phenolic antioxidant compound. Oxidative stress represents one of the important mechanisms underlying ischemia–reperfusion-induced kidney injury. The aim of this study was to investigate the effect of tyrosol against ischemia–reperfusion-induced acute kidney injury. The left kidney of Sprague–Dawley rats was subjected to 45 min of ischemia followed by reperfusion for 6 h. Ischemia–reperfusion caused an increase in peroxynitrite formation and lipid peroxidation. The level of nitric oxide (NO) metabolites and the mRNA of inducible nitric oxide synthase (iNOS) were elevated in ischemia-reperfused kidneys. Administration of tyrosol (100 mg/kg body weight) to rats prior to the induction of ischemia significantly reduced peroxynitrite formation, lipid peroxidation, and the level of NO metabolites. Tyrosol administration also attenuated ischemia–reperfusion-induced NF-κB activation and iNOS expression. Such a treatment improved kidney function. Results suggest that tyrosol may have a protective effect against acute kidney injury through inhibition of iNOS-mediated oxidative stress.</abstract><cop>Washington, DC</cop><pub>American Chemical Society</pub><pmid>23566115</pmid><doi>10.1021/jf400227u</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Antioxidants - administration & dosage Antioxidants - therapeutic use Biological and medical sciences body weight Dose-Response Relationship, Drug Down-Regulation - drug effects Food industries Fundamental and applied biological sciences. Psychology Injections, Intraperitoneal ischemia Kidney - blood supply Kidney - drug effects Kidney - metabolism Kidney - physiopathology kidneys lipid peroxidation Lipid Peroxidation - drug effects Male messenger RNA metabolites nitric oxide Nitric Oxide - metabolism nitric oxide synthase Nitric Oxide Synthase Type II - genetics Nitric Oxide Synthase Type II - metabolism oxidative stress Oxidative Stress - drug effects Phenylethyl Alcohol - administration & dosage Phenylethyl Alcohol - analogs & derivatives Phenylethyl Alcohol - therapeutic use protective effect Rats Rats, Sprague-Dawley renal function Reperfusion Injury - metabolism Reperfusion Injury - physiopathology Reperfusion Injury - prevention & control RNA, Messenger - metabolism |
| title | Tyrosol Attenuates Ischemia–Reperfusion-Induced Kidney Injury via Inhibition of Inducible Nitric Oxide Synthase |
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