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Effects of rebamipide on nephrotoxicity associated with selected NSAIDs in rats
Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is primarily limited by renal and gastrointestinal adverse effects. Rebamipide suppresses gastric mucosal injury when administered with NSAIDs. This study aimed to determine rebamipide's influence upon renal effects following concomitant use...
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| Published in: | European journal of pharmacology 2013-11, Vol.720 (1-3), p.138-146 |
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| container_title | European journal of pharmacology |
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| creator | Wood, Robert C. Wyatt, Jarrett E. Bullins, Kenny W. Hanley, Angela V. Hanley, Gregory A. Denham, James W. Panus, Peter C. Harirforoosh, Sam |
| description | Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is primarily limited by renal and gastrointestinal adverse effects. Rebamipide suppresses gastric mucosal injury when administered with NSAIDs. This study aimed to determine rebamipide's influence upon renal effects following concomitant use with celecoxib or diclofenac. On day 0, rats were randomly divided into 6 groups (n≥6). On days 1 and 2, three groups received placebo and three groups were administered rebamipide (30mg/kg) twice daily. On day 3, the rats treated with placebo received another dose of placebo and ten minutes later a single dose of celecoxib (40mg/kg), diclofenac (10mg/kg), or placebo, respectively. The rats treated with rebamipide received one more dose of rebamipide and ten minutes later one single dose of celecoxib, diclofenac, or placebo, respectively. Urine and blood samples were collected on days 0, 2, and 3. Sodium and potassium excretion rates decreased significantly in the rats treated with celecoxib, diclofenac, rebamipide plus celecoxib, or rebamipide plus diclofenac on day 3. Blood urea nitrogen (BUN) levels significantly increased in placebo plus diclofenac and rebamipide plus diclofenac groups on day 3. Comparing the two groups, the levels of BUN was significantly higher in the rebamipide plus diclofenac group compared to that of placebo plus diclofenac group. Concomitant administration of rebamipide with either NSAID caused a rise in concentrations of urinary kidney injury molecule-1. Histopathological evaluations revealed an intensified NSAID-induced tubular necrosis by rebamipide. Based upon the results obtained, concomitant administration of rebamipide with NSAIDs enhances the effect of NSAIDs on tubular injury. |
| doi_str_mv | 10.1016/j.ejphar.2013.10.035 |
| format | article |
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Rebamipide suppresses gastric mucosal injury when administered with NSAIDs. This study aimed to determine rebamipide's influence upon renal effects following concomitant use with celecoxib or diclofenac. On day 0, rats were randomly divided into 6 groups (n≥6). On days 1 and 2, three groups received placebo and three groups were administered rebamipide (30mg/kg) twice daily. On day 3, the rats treated with placebo received another dose of placebo and ten minutes later a single dose of celecoxib (40mg/kg), diclofenac (10mg/kg), or placebo, respectively. The rats treated with rebamipide received one more dose of rebamipide and ten minutes later one single dose of celecoxib, diclofenac, or placebo, respectively. Urine and blood samples were collected on days 0, 2, and 3. Sodium and potassium excretion rates decreased significantly in the rats treated with celecoxib, diclofenac, rebamipide plus celecoxib, or rebamipide plus diclofenac on day 3. Blood urea nitrogen (BUN) levels significantly increased in placebo plus diclofenac and rebamipide plus diclofenac groups on day 3. Comparing the two groups, the levels of BUN was significantly higher in the rebamipide plus diclofenac group compared to that of placebo plus diclofenac group. Concomitant administration of rebamipide with either NSAID caused a rise in concentrations of urinary kidney injury molecule-1. Histopathological evaluations revealed an intensified NSAID-induced tubular necrosis by rebamipide. Based upon the results obtained, concomitant administration of rebamipide with NSAIDs enhances the effect of NSAIDs on tubular injury.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2013.10.035</identifier><identifier>PMID: 24365796</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>adverse effects ; Alanine - analogs & derivatives ; Alanine - pharmacology ; Animals ; Anti-Inflammatory Agents, Non-Steroidal - adverse effects ; Anti-Ulcer Agents - pharmacology ; blood ; Celecoxib ; Cell Adhesion Molecules - urine ; Creatinine - urine ; Cyclooxygenase ; Diclofenac - adverse effects ; Dinoprostone - blood ; Drug Interactions ; Electrolyte ; excretion ; gastrointestinal system ; histopathology ; Kidney ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Kidney Diseases - blood ; Kidney Diseases - chemically induced ; Kidney Diseases - pathology ; Kidney Diseases - urine ; kidneys ; Male ; necrosis ; nephrotoxicity ; Nitric Oxide - blood ; nonsteroidal anti-inflammatory agents ; NSAIDs ; potassium ; Potassium - urine ; Prostaglandin ; Pyrazoles - adverse effects ; Quinolones - pharmacology ; Rats ; Rats, Sprague-Dawley ; Rebamipide ; sodium ; Sodium - urine ; Sulfonamides - adverse effects ; urea nitrogen ; urine</subject><ispartof>European journal of pharmacology, 2013-11, Vol.720 (1-3), p.138-146</ispartof><rights>2013 Elsevier B.V.</rights><rights>2013 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-c62aa17a18dc3b1de2bbeb35c12ed0bd6988a25207d724c51d9bb792d54a962e3</citedby><cites>FETCH-LOGICAL-c419t-c62aa17a18dc3b1de2bbeb35c12ed0bd6988a25207d724c51d9bb792d54a962e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24365796$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wood, Robert C.</creatorcontrib><creatorcontrib>Wyatt, Jarrett E.</creatorcontrib><creatorcontrib>Bullins, Kenny W.</creatorcontrib><creatorcontrib>Hanley, Angela V.</creatorcontrib><creatorcontrib>Hanley, Gregory A.</creatorcontrib><creatorcontrib>Denham, James W.</creatorcontrib><creatorcontrib>Panus, Peter C.</creatorcontrib><creatorcontrib>Harirforoosh, Sam</creatorcontrib><title>Effects of rebamipide on nephrotoxicity associated with selected NSAIDs in rats</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is primarily limited by renal and gastrointestinal adverse effects. Rebamipide suppresses gastric mucosal injury when administered with NSAIDs. This study aimed to determine rebamipide's influence upon renal effects following concomitant use with celecoxib or diclofenac. On day 0, rats were randomly divided into 6 groups (n≥6). On days 1 and 2, three groups received placebo and three groups were administered rebamipide (30mg/kg) twice daily. On day 3, the rats treated with placebo received another dose of placebo and ten minutes later a single dose of celecoxib (40mg/kg), diclofenac (10mg/kg), or placebo, respectively. The rats treated with rebamipide received one more dose of rebamipide and ten minutes later one single dose of celecoxib, diclofenac, or placebo, respectively. Urine and blood samples were collected on days 0, 2, and 3. Sodium and potassium excretion rates decreased significantly in the rats treated with celecoxib, diclofenac, rebamipide plus celecoxib, or rebamipide plus diclofenac on day 3. Blood urea nitrogen (BUN) levels significantly increased in placebo plus diclofenac and rebamipide plus diclofenac groups on day 3. Comparing the two groups, the levels of BUN was significantly higher in the rebamipide plus diclofenac group compared to that of placebo plus diclofenac group. Concomitant administration of rebamipide with either NSAID caused a rise in concentrations of urinary kidney injury molecule-1. Histopathological evaluations revealed an intensified NSAID-induced tubular necrosis by rebamipide. Based upon the results obtained, concomitant administration of rebamipide with NSAIDs enhances the effect of NSAIDs on tubular injury.</description><subject>adverse effects</subject><subject>Alanine - analogs & derivatives</subject><subject>Alanine - pharmacology</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents, Non-Steroidal - adverse effects</subject><subject>Anti-Ulcer Agents - pharmacology</subject><subject>blood</subject><subject>Celecoxib</subject><subject>Cell Adhesion Molecules - urine</subject><subject>Creatinine - urine</subject><subject>Cyclooxygenase</subject><subject>Diclofenac - adverse effects</subject><subject>Dinoprostone - blood</subject><subject>Drug Interactions</subject><subject>Electrolyte</subject><subject>excretion</subject><subject>gastrointestinal system</subject><subject>histopathology</subject><subject>Kidney</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidney Diseases - blood</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - pathology</subject><subject>Kidney Diseases - urine</subject><subject>kidneys</subject><subject>Male</subject><subject>necrosis</subject><subject>nephrotoxicity</subject><subject>Nitric Oxide - blood</subject><subject>nonsteroidal anti-inflammatory agents</subject><subject>NSAIDs</subject><subject>potassium</subject><subject>Potassium - urine</subject><subject>Prostaglandin</subject><subject>Pyrazoles - adverse effects</subject><subject>Quinolones - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rebamipide</subject><subject>sodium</subject><subject>Sodium - urine</subject><subject>Sulfonamides - adverse effects</subject><subject>urea nitrogen</subject><subject>urine</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqFkctOHDEQRa0oURgef4DAy2x64me7vYmECCFIKCwIa8uPasajmXZj95Dw9_GoCctkVXLp3KrSMUKnlCwpoe3n9RLW48rmJSOU19aScPkOLWindEMUZe_RghAqGqa1PkCHpawJIVIz-REdMMFbqXS7QHdXfQ9-Kjj1OIOz2zjGADgNeIBxldOUfkcfpxdsS0k-2gkC_hWnFS6wqbn6-nF_cfO14DjgbKdyjD70dlPg5LUeoYdvVz8vvze3d9c3lxe3jRdUT41vmbVUWdoFzx0NwJwDx6WnDAJxodVdZ5lkRAXFhJc0aOeUZkEKq1sG_Ah9mueOOT3toExmG4uHzcYOkHbF0I4rLrhqyf9RoYmStOWsomJGfU6lZOjNmOPW5hdDidlbN2szWzd76_tutV5jZ68bdm4L4S30V3MFzmegt8nYxxyLebivE2T9EkGV5pX4MhNQpT1HyKb4CIOHEHP1bEKK_77hD8iPndM</recordid><startdate>20131115</startdate><enddate>20131115</enddate><creator>Wood, Robert C.</creator><creator>Wyatt, Jarrett E.</creator><creator>Bullins, Kenny W.</creator><creator>Hanley, Angela V.</creator><creator>Hanley, Gregory A.</creator><creator>Denham, James W.</creator><creator>Panus, Peter C.</creator><creator>Harirforoosh, Sam</creator><general>Elsevier B.V</general><scope>FBQ</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><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20131115</creationdate><title>Effects of rebamipide on nephrotoxicity associated with selected NSAIDs in rats</title><author>Wood, Robert C. ; Wyatt, Jarrett E. ; Bullins, Kenny W. ; Hanley, Angela V. ; Hanley, Gregory A. ; Denham, James W. ; Panus, Peter C. ; Harirforoosh, Sam</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-c62aa17a18dc3b1de2bbeb35c12ed0bd6988a25207d724c51d9bb792d54a962e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>adverse effects</topic><topic>Alanine - analogs & derivatives</topic><topic>Alanine - pharmacology</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents, Non-Steroidal - adverse effects</topic><topic>Anti-Ulcer Agents - pharmacology</topic><topic>blood</topic><topic>Celecoxib</topic><topic>Cell Adhesion Molecules - urine</topic><topic>Creatinine - urine</topic><topic>Cyclooxygenase</topic><topic>Diclofenac - adverse effects</topic><topic>Dinoprostone - blood</topic><topic>Drug Interactions</topic><topic>Electrolyte</topic><topic>excretion</topic><topic>gastrointestinal system</topic><topic>histopathology</topic><topic>Kidney</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidney Diseases - blood</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - pathology</topic><topic>Kidney Diseases - urine</topic><topic>kidneys</topic><topic>Male</topic><topic>necrosis</topic><topic>nephrotoxicity</topic><topic>Nitric Oxide - blood</topic><topic>nonsteroidal anti-inflammatory agents</topic><topic>NSAIDs</topic><topic>potassium</topic><topic>Potassium - urine</topic><topic>Prostaglandin</topic><topic>Pyrazoles - adverse effects</topic><topic>Quinolones - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rebamipide</topic><topic>sodium</topic><topic>Sodium - urine</topic><topic>Sulfonamides - adverse effects</topic><topic>urea nitrogen</topic><topic>urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wood, Robert C.</creatorcontrib><creatorcontrib>Wyatt, Jarrett E.</creatorcontrib><creatorcontrib>Bullins, Kenny W.</creatorcontrib><creatorcontrib>Hanley, Angela V.</creatorcontrib><creatorcontrib>Hanley, Gregory A.</creatorcontrib><creatorcontrib>Denham, James W.</creatorcontrib><creatorcontrib>Panus, Peter C.</creatorcontrib><creatorcontrib>Harirforoosh, Sam</creatorcontrib><collection>AGRIS</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><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wood, Robert C.</au><au>Wyatt, Jarrett E.</au><au>Bullins, Kenny W.</au><au>Hanley, Angela V.</au><au>Hanley, Gregory A.</au><au>Denham, James W.</au><au>Panus, Peter C.</au><au>Harirforoosh, Sam</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of rebamipide on nephrotoxicity associated with selected NSAIDs in rats</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2013-11-15</date><risdate>2013</risdate><volume>720</volume><issue>1-3</issue><spage>138</spage><epage>146</epage><pages>138-146</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><abstract>Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is primarily limited by renal and gastrointestinal adverse effects. Rebamipide suppresses gastric mucosal injury when administered with NSAIDs. This study aimed to determine rebamipide's influence upon renal effects following concomitant use with celecoxib or diclofenac. On day 0, rats were randomly divided into 6 groups (n≥6). On days 1 and 2, three groups received placebo and three groups were administered rebamipide (30mg/kg) twice daily. On day 3, the rats treated with placebo received another dose of placebo and ten minutes later a single dose of celecoxib (40mg/kg), diclofenac (10mg/kg), or placebo, respectively. The rats treated with rebamipide received one more dose of rebamipide and ten minutes later one single dose of celecoxib, diclofenac, or placebo, respectively. Urine and blood samples were collected on days 0, 2, and 3. Sodium and potassium excretion rates decreased significantly in the rats treated with celecoxib, diclofenac, rebamipide plus celecoxib, or rebamipide plus diclofenac on day 3. Blood urea nitrogen (BUN) levels significantly increased in placebo plus diclofenac and rebamipide plus diclofenac groups on day 3. Comparing the two groups, the levels of BUN was significantly higher in the rebamipide plus diclofenac group compared to that of placebo plus diclofenac group. Concomitant administration of rebamipide with either NSAID caused a rise in concentrations of urinary kidney injury molecule-1. Histopathological evaluations revealed an intensified NSAID-induced tubular necrosis by rebamipide. Based upon the results obtained, concomitant administration of rebamipide with NSAIDs enhances the effect of NSAIDs on tubular injury.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>24365796</pmid><doi>10.1016/j.ejphar.2013.10.035</doi><tpages>9</tpages></addata></record> |
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| source | Elsevier |
| subjects | adverse effects Alanine - analogs & derivatives Alanine - pharmacology Animals Anti-Inflammatory Agents, Non-Steroidal - adverse effects Anti-Ulcer Agents - pharmacology blood Celecoxib Cell Adhesion Molecules - urine Creatinine - urine Cyclooxygenase Diclofenac - adverse effects Dinoprostone - blood Drug Interactions Electrolyte excretion gastrointestinal system histopathology Kidney Kidney - drug effects Kidney - metabolism Kidney - pathology Kidney Diseases - blood Kidney Diseases - chemically induced Kidney Diseases - pathology Kidney Diseases - urine kidneys Male necrosis nephrotoxicity Nitric Oxide - blood nonsteroidal anti-inflammatory agents NSAIDs potassium Potassium - urine Prostaglandin Pyrazoles - adverse effects Quinolones - pharmacology Rats Rats, Sprague-Dawley Rebamipide sodium Sodium - urine Sulfonamides - adverse effects urea nitrogen urine |
| title | Effects of rebamipide on nephrotoxicity associated with selected NSAIDs in rats |
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