Renoprotective potency of amifostine in rat renal ischaemia–reperfusion
Purpose. Kidneys from haemodynamically unstable donors may suffer from renal ischaemia–reperfusion (RIR) injury. RIR is associated with reactive oxygen species production that induces inflammation and activates the arachidonic acid (AA) pathway which converts AA into prostaglandin E2. Amifostine was...
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| Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 2010-12, Vol.25 (12), p.3845-3851 |
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| creator | Chok, Mohammed Koussai Conti, Marc Almolki, Abdelhamid Ferlicot, Sophie Loric, Sylvain Dürrbach, Antoine Benoît, Gérard Droupy, Stéphane Eschwège, Pascal |
| description | Purpose. Kidneys from haemodynamically unstable donors may suffer from renal ischaemia–reperfusion (RIR) injury. RIR is associated with reactive oxygen species production that induces inflammation and activates the arachidonic acid (AA) pathway which converts AA into prostaglandin E2. Amifostine was investigated for its renoprotective potential in RIR. Materials and methods. The effect of amifostine (25 mg/kg = 910 mg/m2) on the COX pathway, enzymatic antioxidant activity, the lipid peroxidation marker MDA, serum creatinine and apoptosis was determined in rats. Kidneys were subjected to 45 min of ischaemia and 1 or 24 h of reperfusion. Control groups (sham: coeliotomy, no ischaemia; r1: 45 min ischaemia/1 h reperfusion; r2: 45 min ischaemia/24 h reperfusion) were administered physiological saline intraperitoneally, and treated groups (E1: 45 min ischaemia/1 h reperfusion; E2: 45 min ischaemia/24 h reperfusion) received amifostine 30 min before reperfusion. Results. Serum creatinine increased in non-treated control rats: r1 vs sham (1.6-fold; P |
| doi_str_mv | 10.1093/ndt/gfq314 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_812137109</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>812137109</sourcerecordid><originalsourceid>FETCH-LOGICAL-c386t-f95c4efc027a84bfa3f7c8d57e65ad19bbd6ddbd032acff5fed86a238b7d1eae3</originalsourceid><addsrcrecordid>eNpF0MFOGzEQBmCrAjUh7aUPgPaCkJC22Ot4vXsEBA0VqFKaSlEv1qw9pi673mBvULnxDrxhnwSjBDjNSPNpNPMT8oXRr4zW_Nib4fjG3nE2_UDGbFrSvOCV2CHjNGQ5FbQekb0Y_1JK60LKj2RUUFGIWooxuZyj71ehH1AP7h6zVeq8fsh6m0HnbB8H5zFzPgswZAE9tJmL-g9g5-D_41PAFQa7jq73n8iuhTbi522dkF8X54uzWX7149vl2clVrnlVDrmthZ6i1bSQUE0bC9xKXRkhsRRgWN00pjSmMZQXoK0VFk1VQnqokYYhIJ-Qw83edPXdGuOgunQRti147NdRVaxgXL4EMyFHG6lDH2NAq1bBdRAeFKPqBaiUnNokl_D-du266dC80deoEjjYAogaWhvAaxffHS8FY7xILt84Fwf89zaHcKtKyaVQs-Vv9f10Of-5vK7Ugj8D0-SKZQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>812137109</pqid></control><display><type>article</type><title>Renoprotective potency of amifostine in rat renal ischaemia–reperfusion</title><source>MEDLINE</source><source>Oxford University Press Journals All Titles (1996-Current)</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Chok, Mohammed Koussai ; Conti, Marc ; Almolki, Abdelhamid ; Ferlicot, Sophie ; Loric, Sylvain ; Dürrbach, Antoine ; Benoît, Gérard ; Droupy, Stéphane ; Eschwège, Pascal</creator><creatorcontrib>Chok, Mohammed Koussai ; Conti, Marc ; Almolki, Abdelhamid ; Ferlicot, Sophie ; Loric, Sylvain ; Dürrbach, Antoine ; Benoît, Gérard ; Droupy, Stéphane ; Eschwège, Pascal</creatorcontrib><description><![CDATA[Purpose. Kidneys from haemodynamically unstable donors may suffer from renal ischaemia–reperfusion (RIR) injury. RIR is associated with reactive oxygen species production that induces inflammation and activates the arachidonic acid (AA) pathway which converts AA into prostaglandin E2. Amifostine was investigated for its renoprotective potential in RIR. Materials and methods. The effect of amifostine (25 mg/kg = 910 mg/m2) on the COX pathway, enzymatic antioxidant activity, the lipid peroxidation marker MDA, serum creatinine and apoptosis was determined in rats. Kidneys were subjected to 45 min of ischaemia and 1 or 24 h of reperfusion. Control groups (sham: coeliotomy, no ischaemia; r1: 45 min ischaemia/1 h reperfusion; r2: 45 min ischaemia/24 h reperfusion) were administered physiological saline intraperitoneally, and treated groups (E1: 45 min ischaemia/1 h reperfusion; E2: 45 min ischaemia/24 h reperfusion) received amifostine 30 min before reperfusion. Results. Serum creatinine increased in non-treated control rats: r1 vs sham (1.6-fold; P <0.007), r2 vs sham (2-fold; P <0.007). Amifostine decreased serum creatinine levels in treated rats: E1 vs r1 (8%; P <0.0025), E2 vs r2 (44%; P <0.0025). Amifostine reduced acute tubular necrosis (25%) 24 h after reperfusion: E1 vs r1 (P <0.004), E2 vs r2 (P <0.03) and reduced COX-2 and microsomal prostaglandin E synthase expression: E1 vs r1 (P <0.03), E2 vs r2 (P <0.02). Amifostine decreased MDA (P <0.04) and reduced caspase-3 expression but did not alter enzymatic antioxidant activity after RIR. Conclusions. Amifostine decreased the degree and severity of tubular damage after reperfusion, probably by scavenging oxygen free radicals and attenuating the cytotoxic effects of inflammatory infiltrates and apoptosis.]]></description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfq314</identifier><identifier>PMID: 20525975</identifier><identifier>CODEN: NDTREA</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Acute Kidney Injury - metabolism ; Acute Kidney Injury - pathology ; Acute Kidney Injury - prevention & control ; amifostine ; Amifostine - pharmacology ; Amifostine - therapeutic use ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Animals ; Biological and medical sciences ; Creatinine - blood ; cyclooxygenase ; Cyclooxygenase 2 - metabolism ; Emergency and intensive care: renal failure. Dialysis management ; Intensive care medicine ; Intramolecular Oxidoreductases - metabolism ; ischaemia–reperfusion ; kidney ; Kidney Tubules - blood supply ; Kidney Tubules - metabolism ; Kidney Tubules - pathology ; Lipid Peroxidation - drug effects ; Male ; Medical sciences ; Models, Animal ; Necrosis ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Prostaglandin-E Synthases ; Rats ; Rats, Sprague-Dawley ; reactive oxygen species ; Reactive Oxygen Species - metabolism ; Renal failure ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Reperfusion Injury - prevention & control ; Treatment Outcome</subject><ispartof>Nephrology, dialysis, transplantation, 2010-12, Vol.25 (12), p.3845-3851</ispartof><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c386t-f95c4efc027a84bfa3f7c8d57e65ad19bbd6ddbd032acff5fed86a238b7d1eae3</citedby><cites>FETCH-LOGICAL-c386t-f95c4efc027a84bfa3f7c8d57e65ad19bbd6ddbd032acff5fed86a238b7d1eae3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23651132$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20525975$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chok, Mohammed Koussai</creatorcontrib><creatorcontrib>Conti, Marc</creatorcontrib><creatorcontrib>Almolki, Abdelhamid</creatorcontrib><creatorcontrib>Ferlicot, Sophie</creatorcontrib><creatorcontrib>Loric, Sylvain</creatorcontrib><creatorcontrib>Dürrbach, Antoine</creatorcontrib><creatorcontrib>Benoît, Gérard</creatorcontrib><creatorcontrib>Droupy, Stéphane</creatorcontrib><creatorcontrib>Eschwège, Pascal</creatorcontrib><title>Renoprotective potency of amifostine in rat renal ischaemia–reperfusion</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol Dial Transplant</addtitle><description><![CDATA[Purpose. Kidneys from haemodynamically unstable donors may suffer from renal ischaemia–reperfusion (RIR) injury. RIR is associated with reactive oxygen species production that induces inflammation and activates the arachidonic acid (AA) pathway which converts AA into prostaglandin E2. Amifostine was investigated for its renoprotective potential in RIR. Materials and methods. The effect of amifostine (25 mg/kg = 910 mg/m2) on the COX pathway, enzymatic antioxidant activity, the lipid peroxidation marker MDA, serum creatinine and apoptosis was determined in rats. Kidneys were subjected to 45 min of ischaemia and 1 or 24 h of reperfusion. Control groups (sham: coeliotomy, no ischaemia; r1: 45 min ischaemia/1 h reperfusion; r2: 45 min ischaemia/24 h reperfusion) were administered physiological saline intraperitoneally, and treated groups (E1: 45 min ischaemia/1 h reperfusion; E2: 45 min ischaemia/24 h reperfusion) received amifostine 30 min before reperfusion. Results. Serum creatinine increased in non-treated control rats: r1 vs sham (1.6-fold; P <0.007), r2 vs sham (2-fold; P <0.007). Amifostine decreased serum creatinine levels in treated rats: E1 vs r1 (8%; P <0.0025), E2 vs r2 (44%; P <0.0025). Amifostine reduced acute tubular necrosis (25%) 24 h after reperfusion: E1 vs r1 (P <0.004), E2 vs r2 (P <0.03) and reduced COX-2 and microsomal prostaglandin E synthase expression: E1 vs r1 (P <0.03), E2 vs r2 (P <0.02). Amifostine decreased MDA (P <0.04) and reduced caspase-3 expression but did not alter enzymatic antioxidant activity after RIR. Conclusions. Amifostine decreased the degree and severity of tubular damage after reperfusion, probably by scavenging oxygen free radicals and attenuating the cytotoxic effects of inflammatory infiltrates and apoptosis.]]></description><subject>Acute Kidney Injury - metabolism</subject><subject>Acute Kidney Injury - pathology</subject><subject>Acute Kidney Injury - prevention & control</subject><subject>amifostine</subject><subject>Amifostine - pharmacology</subject><subject>Amifostine - therapeutic use</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Creatinine - blood</subject><subject>cyclooxygenase</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Intensive care medicine</subject><subject>Intramolecular Oxidoreductases - metabolism</subject><subject>ischaemia–reperfusion</subject><subject>kidney</subject><subject>Kidney Tubules - blood supply</subject><subject>Kidney Tubules - metabolism</subject><subject>Kidney Tubules - pathology</subject><subject>Lipid Peroxidation - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Models, Animal</subject><subject>Necrosis</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Prostaglandin-E Synthases</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Renal failure</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Treatment Outcome</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0MFOGzEQBmCrAjUh7aUPgPaCkJC22Ot4vXsEBA0VqFKaSlEv1qw9pi673mBvULnxDrxhnwSjBDjNSPNpNPMT8oXRr4zW_Nib4fjG3nE2_UDGbFrSvOCV2CHjNGQ5FbQekb0Y_1JK60LKj2RUUFGIWooxuZyj71ehH1AP7h6zVeq8fsh6m0HnbB8H5zFzPgswZAE9tJmL-g9g5-D_41PAFQa7jq73n8iuhTbi522dkF8X54uzWX7149vl2clVrnlVDrmthZ6i1bSQUE0bC9xKXRkhsRRgWN00pjSmMZQXoK0VFk1VQnqokYYhIJ-Qw83edPXdGuOgunQRti147NdRVaxgXL4EMyFHG6lDH2NAq1bBdRAeFKPqBaiUnNokl_D-du266dC80deoEjjYAogaWhvAaxffHS8FY7xILt84Fwf89zaHcKtKyaVQs-Vv9f10Of-5vK7Ugj8D0-SKZQ</recordid><startdate>20101201</startdate><enddate>20101201</enddate><creator>Chok, Mohammed Koussai</creator><creator>Conti, Marc</creator><creator>Almolki, Abdelhamid</creator><creator>Ferlicot, Sophie</creator><creator>Loric, Sylvain</creator><creator>Dürrbach, Antoine</creator><creator>Benoît, Gérard</creator><creator>Droupy, Stéphane</creator><creator>Eschwège, Pascal</creator><general>Oxford University Press</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><scope>7X8</scope></search><sort><creationdate>20101201</creationdate><title>Renoprotective potency of amifostine in rat renal ischaemia–reperfusion</title><author>Chok, Mohammed Koussai ; Conti, Marc ; Almolki, Abdelhamid ; Ferlicot, Sophie ; Loric, Sylvain ; Dürrbach, Antoine ; Benoît, Gérard ; Droupy, Stéphane ; Eschwège, Pascal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c386t-f95c4efc027a84bfa3f7c8d57e65ad19bbd6ddbd032acff5fed86a238b7d1eae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Acute Kidney Injury - metabolism</topic><topic>Acute Kidney Injury - pathology</topic><topic>Acute Kidney Injury - prevention & control</topic><topic>amifostine</topic><topic>Amifostine - pharmacology</topic><topic>Amifostine - therapeutic use</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Creatinine - blood</topic><topic>cyclooxygenase</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Intensive care medicine</topic><topic>Intramolecular Oxidoreductases - metabolism</topic><topic>ischaemia–reperfusion</topic><topic>kidney</topic><topic>Kidney Tubules - blood supply</topic><topic>Kidney Tubules - metabolism</topic><topic>Kidney Tubules - pathology</topic><topic>Lipid Peroxidation - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Models, Animal</topic><topic>Necrosis</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Prostaglandin-E Synthases</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Renal failure</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chok, Mohammed Koussai</creatorcontrib><creatorcontrib>Conti, Marc</creatorcontrib><creatorcontrib>Almolki, Abdelhamid</creatorcontrib><creatorcontrib>Ferlicot, Sophie</creatorcontrib><creatorcontrib>Loric, Sylvain</creatorcontrib><creatorcontrib>Dürrbach, Antoine</creatorcontrib><creatorcontrib>Benoît, Gérard</creatorcontrib><creatorcontrib>Droupy, Stéphane</creatorcontrib><creatorcontrib>Eschwège, Pascal</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><collection>MEDLINE - Academic</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chok, Mohammed Koussai</au><au>Conti, Marc</au><au>Almolki, Abdelhamid</au><au>Ferlicot, Sophie</au><au>Loric, Sylvain</au><au>Dürrbach, Antoine</au><au>Benoît, Gérard</au><au>Droupy, Stéphane</au><au>Eschwège, Pascal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Renoprotective potency of amifostine in rat renal ischaemia–reperfusion</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><addtitle>Nephrol Dial Transplant</addtitle><date>2010-12-01</date><risdate>2010</risdate><volume>25</volume><issue>12</issue><spage>3845</spage><epage>3851</epage><pages>3845-3851</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><coden>NDTREA</coden><abstract><![CDATA[Purpose. Kidneys from haemodynamically unstable donors may suffer from renal ischaemia–reperfusion (RIR) injury. RIR is associated with reactive oxygen species production that induces inflammation and activates the arachidonic acid (AA) pathway which converts AA into prostaglandin E2. Amifostine was investigated for its renoprotective potential in RIR. Materials and methods. The effect of amifostine (25 mg/kg = 910 mg/m2) on the COX pathway, enzymatic antioxidant activity, the lipid peroxidation marker MDA, serum creatinine and apoptosis was determined in rats. Kidneys were subjected to 45 min of ischaemia and 1 or 24 h of reperfusion. Control groups (sham: coeliotomy, no ischaemia; r1: 45 min ischaemia/1 h reperfusion; r2: 45 min ischaemia/24 h reperfusion) were administered physiological saline intraperitoneally, and treated groups (E1: 45 min ischaemia/1 h reperfusion; E2: 45 min ischaemia/24 h reperfusion) received amifostine 30 min before reperfusion. Results. Serum creatinine increased in non-treated control rats: r1 vs sham (1.6-fold; P <0.007), r2 vs sham (2-fold; P <0.007). Amifostine decreased serum creatinine levels in treated rats: E1 vs r1 (8%; P <0.0025), E2 vs r2 (44%; P <0.0025). Amifostine reduced acute tubular necrosis (25%) 24 h after reperfusion: E1 vs r1 (P <0.004), E2 vs r2 (P <0.03) and reduced COX-2 and microsomal prostaglandin E synthase expression: E1 vs r1 (P <0.03), E2 vs r2 (P <0.02). Amifostine decreased MDA (P <0.04) and reduced caspase-3 expression but did not alter enzymatic antioxidant activity after RIR. Conclusions. Amifostine decreased the degree and severity of tubular damage after reperfusion, probably by scavenging oxygen free radicals and attenuating the cytotoxic effects of inflammatory infiltrates and apoptosis.]]></abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>20525975</pmid><doi>10.1093/ndt/gfq314</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Kidney Injury - metabolism Acute Kidney Injury - pathology Acute Kidney Injury - prevention & control amifostine Amifostine - pharmacology Amifostine - therapeutic use Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Animals Biological and medical sciences Creatinine - blood cyclooxygenase Cyclooxygenase 2 - metabolism Emergency and intensive care: renal failure. Dialysis management Intensive care medicine Intramolecular Oxidoreductases - metabolism ischaemia–reperfusion kidney Kidney Tubules - blood supply Kidney Tubules - metabolism Kidney Tubules - pathology Lipid Peroxidation - drug effects Male Medical sciences Models, Animal Necrosis Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Prostaglandin-E Synthases Rats Rats, Sprague-Dawley reactive oxygen species Reactive Oxygen Species - metabolism Renal failure Reperfusion Injury - metabolism Reperfusion Injury - pathology Reperfusion Injury - prevention & control Treatment Outcome |
| title | Renoprotective potency of amifostine in rat renal ischaemia–reperfusion |
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