Which comes first: Renal inflammation or oxidative stress in spontaneously hypertensive rats?
The present study was undertaken to identify whether inflammation or oxidative stress is the primary abnormality in the kidney in spontaneously hypertensive rats (SHR). Renal inflammation and oxidative stress were evaluated in 2- and 3-week-old prehypertensive SHR and age-matched genetically normote...
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Veröffentlicht in: | Free radical research 2007, Vol.41 (2), p.216-224 |
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description | The present study was undertaken to identify whether inflammation or oxidative stress is the primary abnormality in the kidney in spontaneously hypertensive rats (SHR). Renal inflammation and oxidative stress were evaluated in 2- and 3-week-old prehypertensive SHR and age-matched genetically normotensive control Wistar-Kyoto (WKY) rats. Blood pressure was similar in WKY and SHR rats at 2 and 3 weeks, of age. Renal inflammation (macrophage and nuclear factor-κB) was elevated in SHR at 3 weeks, but not at 2 weeks, of age compared with age-matched WKY rats. Renal oxidative stress (nitrotyrosine, 8-hydroxy-2′-deoxyguanosine and p47phox) was also clearly elevated in 3-week-old SHR compared with age-matched WKY rats. Additionally, NADPH oxidase subunit p47phox was found elevated in 2-week-old SHR compared to age-matched WKY rats. Moreover, antioxidant (N-acetyl-l-cysteine and Tempol) treatment reduced renal inflammation in prehypertensive SHR. We therefore conclude that the oxidative stress appears before inflammation as a primary abnormality in the kidney in prehypertensive SHR. |
doi_str_mv | 10.1080/10715760601059672 |
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Renal inflammation and oxidative stress were evaluated in 2- and 3-week-old prehypertensive SHR and age-matched genetically normotensive control Wistar-Kyoto (WKY) rats. Blood pressure was similar in WKY and SHR rats at 2 and 3 weeks, of age. Renal inflammation (macrophage and nuclear factor-κB) was elevated in SHR at 3 weeks, but not at 2 weeks, of age compared with age-matched WKY rats. Renal oxidative stress (nitrotyrosine, 8-hydroxy-2′-deoxyguanosine and p47phox) was also clearly elevated in 3-week-old SHR compared with age-matched WKY rats. Additionally, NADPH oxidase subunit p47phox was found elevated in 2-week-old SHR compared to age-matched WKY rats. Moreover, antioxidant (N-acetyl-l-cysteine and Tempol) treatment reduced renal inflammation in prehypertensive SHR. We therefore conclude that the oxidative stress appears before inflammation as a primary abnormality in the kidney in prehypertensive SHR.</description><identifier>ISSN: 1071-5762</identifier><identifier>EISSN: 1029-2470</identifier><identifier>DOI: 10.1080/10715760601059672</identifier><identifier>PMID: 17364948</identifier><language>eng</language><publisher>England: Informa UK Ltd</publisher><subject>Acetylcysteine - therapeutic use ; Age Factors ; Animals ; Antioxidants - therapeutic use ; Blood Pressure ; Cyclic N-Oxides - therapeutic use ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - analysis ; Disease Models, Animal ; Disease Progression ; DNA Damage ; Glutathione - analysis ; Hypertension - drug therapy ; Hypertension - etiology ; Hypertension - genetics ; Hypertension - metabolism ; inflammation ; Kidney Cortex - metabolism ; Male ; NADPH Oxidases - analysis ; Nephritis - drug therapy ; Nephritis - genetics ; Nephritis - metabolism ; Nephritis - prevention & control ; NF-κBp65 ; nitrotyrosine ; Oxidative Stress ; p47phox ; Rats ; Rats, Inbred SHR - metabolism ; Rats, Inbred WKY ; SHR ; Spin Labels ; Tyrosine - analogs & derivatives ; Tyrosine - analysis</subject><ispartof>Free radical research, 2007, Vol.41 (2), p.216-224</ispartof><rights>2007 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2007</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-9051bbaef085b0515866c6c94e5cad9b14a31b9d63f59c8f58292fa3a2803dee3</citedby><cites>FETCH-LOGICAL-c470t-9051bbaef085b0515866c6c94e5cad9b14a31b9d63f59c8f58292fa3a2803dee3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/10715760601059672$$EPDF$$P50$$Ginformahealthcare$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1080/10715760601059672$$EHTML$$P50$$Ginformahealthcare$$H</linktohtml><link.rule.ids>314,780,784,4024,27923,27924,27925,59647,60436,61221,61402</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17364948$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Biswas, Subrata K.</creatorcontrib><creatorcontrib>Lopes De Faria, Jose B.</creatorcontrib><title>Which comes first: Renal inflammation or oxidative stress in spontaneously hypertensive rats?</title><title>Free radical research</title><addtitle>Free Radic Res</addtitle><description>The present study was undertaken to identify whether inflammation or oxidative stress is the primary abnormality in the kidney in spontaneously hypertensive rats (SHR). Renal inflammation and oxidative stress were evaluated in 2- and 3-week-old prehypertensive SHR and age-matched genetically normotensive control Wistar-Kyoto (WKY) rats. Blood pressure was similar in WKY and SHR rats at 2 and 3 weeks, of age. Renal inflammation (macrophage and nuclear factor-κB) was elevated in SHR at 3 weeks, but not at 2 weeks, of age compared with age-matched WKY rats. Renal oxidative stress (nitrotyrosine, 8-hydroxy-2′-deoxyguanosine and p47phox) was also clearly elevated in 3-week-old SHR compared with age-matched WKY rats. Additionally, NADPH oxidase subunit p47phox was found elevated in 2-week-old SHR compared to age-matched WKY rats. Moreover, antioxidant (N-acetyl-l-cysteine and Tempol) treatment reduced renal inflammation in prehypertensive SHR. We therefore conclude that the oxidative stress appears before inflammation as a primary abnormality in the kidney in prehypertensive SHR.</description><subject>Acetylcysteine - therapeutic use</subject><subject>Age Factors</subject><subject>Animals</subject><subject>Antioxidants - therapeutic use</subject><subject>Blood Pressure</subject><subject>Cyclic N-Oxides - therapeutic use</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - analysis</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>DNA Damage</subject><subject>Glutathione - analysis</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - etiology</subject><subject>Hypertension - genetics</subject><subject>Hypertension - metabolism</subject><subject>inflammation</subject><subject>Kidney Cortex - metabolism</subject><subject>Male</subject><subject>NADPH Oxidases - analysis</subject><subject>Nephritis - drug therapy</subject><subject>Nephritis - genetics</subject><subject>Nephritis - metabolism</subject><subject>Nephritis - prevention & control</subject><subject>NF-κBp65</subject><subject>nitrotyrosine</subject><subject>Oxidative Stress</subject><subject>p47phox</subject><subject>Rats</subject><subject>Rats, Inbred SHR - metabolism</subject><subject>Rats, Inbred WKY</subject><subject>SHR</subject><subject>Spin Labels</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - analysis</subject><issn>1071-5762</issn><issn>1029-2470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kVuLFDEQhYMo7kV_gC-SJ99ac-l0OiqILK4rLAjLik8S0ukK3Uu6M6Yy6vx7M8yAyMI-VRV853A4RcgLzl5z1rM3nGmudMc6xpkynRaPyClnwjSi1ezxfte8qYA4IWeId4xx2Sr9lJxwLbvWtP0p-fF9mv1EfVoAaZgzlrf0BlYX6byG6JbFlTmtNGWa_sxjPX4BxZIBsQIUN2ktboW0xbij024DucCKeyi7gh-ekSfBRYTnx3lOvl1-ur24aq6_fv5y8fG68TVoaQxTfBgcBNaroe6q7zrfedOC8m40A2-d5IMZOxmU8X1QvTAiOOlEz-QIIM_Jq4PvJqefW8Bilxk9xHjIZjUTmsleVJAfQJ8TYoZgN3leXN5Zzuy-U3uv06p5eTTfDguM_xTHEivw_gDUylJe3O-U42iL28WUQ3arn9HKh_zf_SefwMUyeZfB3qVtrr_AB9L9BWJMmFc</recordid><startdate>2007</startdate><enddate>2007</enddate><creator>Biswas, Subrata K.</creator><creator>Lopes De Faria, Jose B.</creator><general>Informa UK Ltd</general><general>Taylor & Francis</general><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>2007</creationdate><title>Which comes first: Renal inflammation or oxidative stress in spontaneously hypertensive rats?</title><author>Biswas, Subrata K. ; Lopes De Faria, Jose B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-9051bbaef085b0515866c6c94e5cad9b14a31b9d63f59c8f58292fa3a2803dee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Acetylcysteine - therapeutic use</topic><topic>Age Factors</topic><topic>Animals</topic><topic>Antioxidants - therapeutic use</topic><topic>Blood Pressure</topic><topic>Cyclic N-Oxides - therapeutic use</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - analysis</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>DNA Damage</topic><topic>Glutathione - analysis</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - etiology</topic><topic>Hypertension - genetics</topic><topic>Hypertension - metabolism</topic><topic>inflammation</topic><topic>Kidney Cortex - metabolism</topic><topic>Male</topic><topic>NADPH Oxidases - analysis</topic><topic>Nephritis - drug therapy</topic><topic>Nephritis - genetics</topic><topic>Nephritis - metabolism</topic><topic>Nephritis - prevention & control</topic><topic>NF-κBp65</topic><topic>nitrotyrosine</topic><topic>Oxidative Stress</topic><topic>p47phox</topic><topic>Rats</topic><topic>Rats, Inbred SHR - metabolism</topic><topic>Rats, Inbred WKY</topic><topic>SHR</topic><topic>Spin Labels</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Biswas, Subrata K.</creatorcontrib><creatorcontrib>Lopes De Faria, Jose B.</creatorcontrib><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>Free radical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Biswas, Subrata K.</au><au>Lopes De Faria, Jose B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Which comes first: Renal inflammation or oxidative stress in spontaneously hypertensive rats?</atitle><jtitle>Free radical research</jtitle><addtitle>Free Radic Res</addtitle><date>2007</date><risdate>2007</risdate><volume>41</volume><issue>2</issue><spage>216</spage><epage>224</epage><pages>216-224</pages><issn>1071-5762</issn><eissn>1029-2470</eissn><abstract>The present study was undertaken to identify whether inflammation or oxidative stress is the primary abnormality in the kidney in spontaneously hypertensive rats (SHR). Renal inflammation and oxidative stress were evaluated in 2- and 3-week-old prehypertensive SHR and age-matched genetically normotensive control Wistar-Kyoto (WKY) rats. Blood pressure was similar in WKY and SHR rats at 2 and 3 weeks, of age. Renal inflammation (macrophage and nuclear factor-κB) was elevated in SHR at 3 weeks, but not at 2 weeks, of age compared with age-matched WKY rats. Renal oxidative stress (nitrotyrosine, 8-hydroxy-2′-deoxyguanosine and p47phox) was also clearly elevated in 3-week-old SHR compared with age-matched WKY rats. Additionally, NADPH oxidase subunit p47phox was found elevated in 2-week-old SHR compared to age-matched WKY rats. Moreover, antioxidant (N-acetyl-l-cysteine and Tempol) treatment reduced renal inflammation in prehypertensive SHR. We therefore conclude that the oxidative stress appears before inflammation as a primary abnormality in the kidney in prehypertensive SHR.</abstract><cop>England</cop><pub>Informa UK Ltd</pub><pmid>17364948</pmid><doi>10.1080/10715760601059672</doi><tpages>9</tpages></addata></record> |
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subjects | Acetylcysteine - therapeutic use Age Factors Animals Antioxidants - therapeutic use Blood Pressure Cyclic N-Oxides - therapeutic use Deoxyguanosine - analogs & derivatives Deoxyguanosine - analysis Disease Models, Animal Disease Progression DNA Damage Glutathione - analysis Hypertension - drug therapy Hypertension - etiology Hypertension - genetics Hypertension - metabolism inflammation Kidney Cortex - metabolism Male NADPH Oxidases - analysis Nephritis - drug therapy Nephritis - genetics Nephritis - metabolism Nephritis - prevention & control NF-κBp65 nitrotyrosine Oxidative Stress p47phox Rats Rats, Inbred SHR - metabolism Rats, Inbred WKY SHR Spin Labels Tyrosine - analogs & derivatives Tyrosine - analysis |
title | Which comes first: Renal inflammation or oxidative stress in spontaneously hypertensive rats? |
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