Protective effect of febuxostat in sepsis-induced liver and kidney injuries after cecal ligation and puncture with the impact of xanthine oxidase, interleukin 1β, and c-Jun N-terminal kinases
Sepsis is one of the most common causes of death among hospitalized patients. Activity of xanthine oxidase (XO), a reactive oxygen species-producing enzyme, is known to be elevated in septic patients. Our aim was to investigate the possible protective role of XO inhibitor, febuxostat (FEB), in a rat...
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| Veröffentlicht in: | Human & experimental toxicology 2020-07, Vol.39 (7), p.906-919 |
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| creator | Ibrahim, YF Fadl, RR Ibrahim, SAE Gayyed, MF Bayoumi, AMA Refaie, MMM |
| description | Sepsis is one of the most common causes of death among hospitalized patients. Activity of xanthine oxidase (XO), a reactive oxygen species-producing enzyme, is known to be elevated in septic patients. Our aim was to investigate the possible protective role of XO inhibitor, febuxostat (FEB), in a rat model of sepsis-induced liver and kidney injures. Adult male albino rats were divided into four groups (n = 12 each): sham control, sham + FEB, cecal ligation and puncture (CLP), and CLP + FEB groups. FEB (10 mg/kg per os (p.o.)) was given once daily for 2 days and 30 min prior to laparotomy with CLP. CLP was associated with a high mortality rate accompanied by significant liver and kidney injuries indicated by elevated serum alanine aminotransferase, aspartate aminotransferase, urea, and creatinine levels and confirmed by histopathological tissue injury. Moreover, there was an increase in neutrophil gelatinase-associated lipocalin, uric acid, malondialdehyde, and nitric oxide levels and with decreased superoxide dismutase activity and total antioxidant capacity. In addition, CLP caused increased expression of the inflammatory markers tumor necrosis factor alpha, interleukin 1beta protein levels, and nuclear factor kappa B immunoexpression. Finally, CLP operated rats exhibited an upregulation in the apoptotic mediators, caspase 3, and P-C-Jun N-terminal kinases (JNK) proteins. FEB treatment of CLP rats caused a significant improvement and normalization in all measured parameters. Moreover, FEB amerliorates degenerative histopathological changes and improves the overall survival rate. In conclusion, FEB exhibited a protective effect in sepsis-induced liver and kidney injuries most probably through its anti-inflammatory, antioxidant, and antiapoptotic properties and attenuating JNK signaling pathway secondary to its XO enzyme inhibitory activity. |
| doi_str_mv | 10.1177/0960327120905957 |
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Activity of xanthine oxidase (XO), a reactive oxygen species-producing enzyme, is known to be elevated in septic patients. Our aim was to investigate the possible protective role of XO inhibitor, febuxostat (FEB), in a rat model of sepsis-induced liver and kidney injures. Adult male albino rats were divided into four groups (n = 12 each): sham control, sham + FEB, cecal ligation and puncture (CLP), and CLP + FEB groups. FEB (10 mg/kg per os (p.o.)) was given once daily for 2 days and 30 min prior to laparotomy with CLP. CLP was associated with a high mortality rate accompanied by significant liver and kidney injuries indicated by elevated serum alanine aminotransferase, aspartate aminotransferase, urea, and creatinine levels and confirmed by histopathological tissue injury. Moreover, there was an increase in neutrophil gelatinase-associated lipocalin, uric acid, malondialdehyde, and nitric oxide levels and with decreased superoxide dismutase activity and total antioxidant capacity. In addition, CLP caused increased expression of the inflammatory markers tumor necrosis factor alpha, interleukin 1beta protein levels, and nuclear factor kappa B immunoexpression. Finally, CLP operated rats exhibited an upregulation in the apoptotic mediators, caspase 3, and P-C-Jun N-terminal kinases (JNK) proteins. FEB treatment of CLP rats caused a significant improvement and normalization in all measured parameters. Moreover, FEB amerliorates degenerative histopathological changes and improves the overall survival rate. In conclusion, FEB exhibited a protective effect in sepsis-induced liver and kidney injuries most probably through its anti-inflammatory, antioxidant, and antiapoptotic properties and attenuating JNK signaling pathway secondary to its XO enzyme inhibitory activity.</description><identifier>ISSN: 0960-3271</identifier><identifier>EISSN: 1477-0903</identifier><identifier>DOI: 10.1177/0960327120905957</identifier><identifier>PMID: 32054342</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Acute Kidney Injury - drug therapy ; Acute Kidney Injury - etiology ; Acute Kidney Injury - metabolism ; Acute Kidney Injury - pathology ; Alanine ; Alanine transaminase ; Alanine Transaminase - blood ; Animals ; Antioxidants ; Apoptosis ; Aspartate aminotransferase ; Aspartate Aminotransferases - blood ; c-Jun protein ; Caspase-3 ; Cecum ; Cecum - surgery ; Creatinine ; Creatinine - blood ; Cytokines ; Enzymes ; Febuxostat - therapeutic use ; Gelatinase ; Inflammation ; Injuries ; Interleukin-1beta - metabolism ; Interleukins ; JNK Mitogen-Activated Protein Kinases - metabolism ; JNK protein ; Kidney - drug effects ; Kidney - metabolism ; Kidney - pathology ; Kidneys ; Kinases ; Ligation ; Lipocalin ; Liver ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; Liver Diseases - drug therapy ; Liver Diseases - etiology ; Liver Diseases - metabolism ; Liver Diseases - pathology ; Male ; Malondialdehyde ; Nitric oxide ; Protective Agents - therapeutic use ; Proteins ; Rats, Wistar ; Reactive oxygen species ; Sepsis ; Sepsis - complications ; Sepsis - drug therapy ; Sepsis - metabolism ; Sepsis - pathology ; Signal transduction ; Superoxide dismutase ; Transcription factors ; Tumor necrosis factor-α ; Urea ; Urea - blood ; Uric acid ; Xanthine oxidase ; Xanthine Oxidase - metabolism</subject><ispartof>Human & experimental toxicology, 2020-07, Vol.39 (7), p.906-919</ispartof><rights>The Author(s) 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-cd625006d23de018bc39edff1a3f18d0a899597384e1df71329a2ddd491597b43</citedby><cites>FETCH-LOGICAL-c365t-cd625006d23de018bc39edff1a3f18d0a899597384e1df71329a2ddd491597b43</cites><orcidid>0000-0001-6082-0295 ; 0000-0003-0216-5020</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0960327120905957$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0960327120905957$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21966,27853,27924,27925,44945,45333</link.rule.ids><linktorsrc>$$Uhttps://journals.sagepub.com/doi/full/10.1177/0960327120905957?utm_source=summon&utm_medium=discovery-provider$$EView_record_in_SAGE_Publications$$FView_record_in_$$GSAGE_Publications</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32054342$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ibrahim, YF</creatorcontrib><creatorcontrib>Fadl, RR</creatorcontrib><creatorcontrib>Ibrahim, SAE</creatorcontrib><creatorcontrib>Gayyed, MF</creatorcontrib><creatorcontrib>Bayoumi, AMA</creatorcontrib><creatorcontrib>Refaie, MMM</creatorcontrib><title>Protective effect of febuxostat in sepsis-induced liver and kidney injuries after cecal ligation and puncture with the impact of xanthine oxidase, interleukin 1β, and c-Jun N-terminal kinases</title><title>Human & experimental toxicology</title><addtitle>Hum Exp Toxicol</addtitle><description>Sepsis is one of the most common causes of death among hospitalized patients. Activity of xanthine oxidase (XO), a reactive oxygen species-producing enzyme, is known to be elevated in septic patients. Our aim was to investigate the possible protective role of XO inhibitor, febuxostat (FEB), in a rat model of sepsis-induced liver and kidney injures. Adult male albino rats were divided into four groups (n = 12 each): sham control, sham + FEB, cecal ligation and puncture (CLP), and CLP + FEB groups. FEB (10 mg/kg per os (p.o.)) was given once daily for 2 days and 30 min prior to laparotomy with CLP. CLP was associated with a high mortality rate accompanied by significant liver and kidney injuries indicated by elevated serum alanine aminotransferase, aspartate aminotransferase, urea, and creatinine levels and confirmed by histopathological tissue injury. Moreover, there was an increase in neutrophil gelatinase-associated lipocalin, uric acid, malondialdehyde, and nitric oxide levels and with decreased superoxide dismutase activity and total antioxidant capacity. In addition, CLP caused increased expression of the inflammatory markers tumor necrosis factor alpha, interleukin 1beta protein levels, and nuclear factor kappa B immunoexpression. Finally, CLP operated rats exhibited an upregulation in the apoptotic mediators, caspase 3, and P-C-Jun N-terminal kinases (JNK) proteins. FEB treatment of CLP rats caused a significant improvement and normalization in all measured parameters. Moreover, FEB amerliorates degenerative histopathological changes and improves the overall survival rate. In conclusion, FEB exhibited a protective effect in sepsis-induced liver and kidney injuries most probably through its anti-inflammatory, antioxidant, and antiapoptotic properties and attenuating JNK signaling pathway secondary to its XO enzyme inhibitory activity.</description><subject>Acute Kidney Injury - drug therapy</subject><subject>Acute Kidney Injury - etiology</subject><subject>Acute Kidney Injury - metabolism</subject><subject>Acute Kidney Injury - pathology</subject><subject>Alanine</subject><subject>Alanine transaminase</subject><subject>Alanine Transaminase - blood</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Aspartate aminotransferase</subject><subject>Aspartate Aminotransferases - blood</subject><subject>c-Jun protein</subject><subject>Caspase-3</subject><subject>Cecum</subject><subject>Cecum - surgery</subject><subject>Creatinine</subject><subject>Creatinine - blood</subject><subject>Cytokines</subject><subject>Enzymes</subject><subject>Febuxostat - therapeutic use</subject><subject>Gelatinase</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Interleukin-1beta - metabolism</subject><subject>Interleukins</subject><subject>JNK Mitogen-Activated Protein Kinases - metabolism</subject><subject>JNK protein</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kidney - pathology</subject><subject>Kidneys</subject><subject>Kinases</subject><subject>Ligation</subject><subject>Lipocalin</subject><subject>Liver</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver Diseases - drug therapy</subject><subject>Liver Diseases - etiology</subject><subject>Liver Diseases - metabolism</subject><subject>Liver Diseases - pathology</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Nitric oxide</subject><subject>Protective Agents - therapeutic use</subject><subject>Proteins</subject><subject>Rats, Wistar</subject><subject>Reactive oxygen species</subject><subject>Sepsis</subject><subject>Sepsis - complications</subject><subject>Sepsis - drug therapy</subject><subject>Sepsis - metabolism</subject><subject>Sepsis - pathology</subject><subject>Signal transduction</subject><subject>Superoxide dismutase</subject><subject>Transcription factors</subject><subject>Tumor necrosis factor-α</subject><subject>Urea</subject><subject>Urea - blood</subject><subject>Uric acid</subject><subject>Xanthine oxidase</subject><subject>Xanthine Oxidase - metabolism</subject><issn>0960-3271</issn><issn>1477-0903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1uEzEUhS1ERUNhzwpZYltTezwzHi9Rxa-qwgLWI8e-bpwmnsE_kL4WT8AT8EzcNC1ISKz8c757jq1DyDPBXwqh1BnXPZeNEg3XvNOdekAWolWK4VE-JIu9zPb6MXmc85pz3utOPCLHsuFdK9tmQX5-SlMBW8I3oOA97ujkqYdl3U25mEJDpBnmHDIL0VULjm6QTdRER6-Di3CDyLqmAJkaX1CxYM0GqStTwhRvwblGW2oC-j2UFS0roGE7m0PWzsSyChHotAvOZDhFP7TZQL3GbPHrx-mthWUfaqSXDKVtiBiAKtL5CTnyZpPh6d16Qr68ef35_B27-Pj2_fmrC2Zl3xVmXd90-H_XSAdcDEsrNTjvhZFeDI6bQetOKzm0IJxXQjbaNM65Vgu8XrbyhLw4-M5p-lohl3E91YQPyWPTcj20qh8kUvxA2TTlnMCPcwpbk25Gwcd9ZeO_leHI8zvjutyC-zNw3xEC7ABkcwV_U_9r-BvYUqHq</recordid><startdate>202007</startdate><enddate>202007</enddate><creator>Ibrahim, YF</creator><creator>Fadl, RR</creator><creator>Ibrahim, SAE</creator><creator>Gayyed, MF</creator><creator>Bayoumi, AMA</creator><creator>Refaie, MMM</creator><general>SAGE Publications</general><general>Sage Publications Ltd</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>7ST</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>SOI</scope><orcidid>https://orcid.org/0000-0001-6082-0295</orcidid><orcidid>https://orcid.org/0000-0003-0216-5020</orcidid></search><sort><creationdate>202007</creationdate><title>Protective effect of febuxostat in sepsis-induced liver and kidney injuries after cecal ligation and puncture with the impact of xanthine oxidase, interleukin 1β, and c-Jun N-terminal kinases</title><author>Ibrahim, YF ; Fadl, RR ; Ibrahim, SAE ; Gayyed, MF ; Bayoumi, AMA ; Refaie, MMM</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-cd625006d23de018bc39edff1a3f18d0a899597384e1df71329a2ddd491597b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acute Kidney Injury - drug therapy</topic><topic>Acute Kidney Injury - etiology</topic><topic>Acute Kidney Injury - metabolism</topic><topic>Acute Kidney Injury - pathology</topic><topic>Alanine</topic><topic>Alanine transaminase</topic><topic>Alanine Transaminase - blood</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Aspartate aminotransferase</topic><topic>Aspartate Aminotransferases - blood</topic><topic>c-Jun protein</topic><topic>Caspase-3</topic><topic>Cecum</topic><topic>Cecum - surgery</topic><topic>Creatinine</topic><topic>Creatinine - blood</topic><topic>Cytokines</topic><topic>Enzymes</topic><topic>Febuxostat - therapeutic use</topic><topic>Gelatinase</topic><topic>Inflammation</topic><topic>Injuries</topic><topic>Interleukin-1beta - metabolism</topic><topic>Interleukins</topic><topic>JNK Mitogen-Activated Protein Kinases - metabolism</topic><topic>JNK protein</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kidney - pathology</topic><topic>Kidneys</topic><topic>Kinases</topic><topic>Ligation</topic><topic>Lipocalin</topic><topic>Liver</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver Diseases - drug therapy</topic><topic>Liver Diseases - etiology</topic><topic>Liver Diseases - metabolism</topic><topic>Liver Diseases - pathology</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Nitric oxide</topic><topic>Protective Agents - therapeutic use</topic><topic>Proteins</topic><topic>Rats, Wistar</topic><topic>Reactive oxygen species</topic><topic>Sepsis</topic><topic>Sepsis - complications</topic><topic>Sepsis - drug therapy</topic><topic>Sepsis - metabolism</topic><topic>Sepsis - pathology</topic><topic>Signal transduction</topic><topic>Superoxide dismutase</topic><topic>Transcription factors</topic><topic>Tumor necrosis factor-α</topic><topic>Urea</topic><topic>Urea - blood</topic><topic>Uric acid</topic><topic>Xanthine oxidase</topic><topic>Xanthine Oxidase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ibrahim, YF</creatorcontrib><creatorcontrib>Fadl, RR</creatorcontrib><creatorcontrib>Ibrahim, SAE</creatorcontrib><creatorcontrib>Gayyed, MF</creatorcontrib><creatorcontrib>Bayoumi, AMA</creatorcontrib><creatorcontrib>Refaie, MMM</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Environment Abstracts</collection><jtitle>Human & experimental toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Ibrahim, YF</au><au>Fadl, RR</au><au>Ibrahim, SAE</au><au>Gayyed, MF</au><au>Bayoumi, AMA</au><au>Refaie, MMM</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Protective effect of febuxostat in sepsis-induced liver and kidney injuries after cecal ligation and puncture with the impact of xanthine oxidase, interleukin 1β, and c-Jun N-terminal kinases</atitle><jtitle>Human & experimental toxicology</jtitle><addtitle>Hum Exp Toxicol</addtitle><date>2020-07</date><risdate>2020</risdate><volume>39</volume><issue>7</issue><spage>906</spage><epage>919</epage><pages>906-919</pages><issn>0960-3271</issn><eissn>1477-0903</eissn><abstract>Sepsis is one of the most common causes of death among hospitalized patients. Activity of xanthine oxidase (XO), a reactive oxygen species-producing enzyme, is known to be elevated in septic patients. Our aim was to investigate the possible protective role of XO inhibitor, febuxostat (FEB), in a rat model of sepsis-induced liver and kidney injures. Adult male albino rats were divided into four groups (n = 12 each): sham control, sham + FEB, cecal ligation and puncture (CLP), and CLP + FEB groups. FEB (10 mg/kg per os (p.o.)) was given once daily for 2 days and 30 min prior to laparotomy with CLP. CLP was associated with a high mortality rate accompanied by significant liver and kidney injuries indicated by elevated serum alanine aminotransferase, aspartate aminotransferase, urea, and creatinine levels and confirmed by histopathological tissue injury. Moreover, there was an increase in neutrophil gelatinase-associated lipocalin, uric acid, malondialdehyde, and nitric oxide levels and with decreased superoxide dismutase activity and total antioxidant capacity. In addition, CLP caused increased expression of the inflammatory markers tumor necrosis factor alpha, interleukin 1beta protein levels, and nuclear factor kappa B immunoexpression. Finally, CLP operated rats exhibited an upregulation in the apoptotic mediators, caspase 3, and P-C-Jun N-terminal kinases (JNK) proteins. FEB treatment of CLP rats caused a significant improvement and normalization in all measured parameters. Moreover, FEB amerliorates degenerative histopathological changes and improves the overall survival rate. In conclusion, FEB exhibited a protective effect in sepsis-induced liver and kidney injuries most probably through its anti-inflammatory, antioxidant, and antiapoptotic properties and attenuating JNK signaling pathway secondary to its XO enzyme inhibitory activity.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>32054342</pmid><doi>10.1177/0960327120905957</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-6082-0295</orcidid><orcidid>https://orcid.org/0000-0003-0216-5020</orcidid></addata></record> |
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| subjects | Acute Kidney Injury - drug therapy Acute Kidney Injury - etiology Acute Kidney Injury - metabolism Acute Kidney Injury - pathology Alanine Alanine transaminase Alanine Transaminase - blood Animals Antioxidants Apoptosis Aspartate aminotransferase Aspartate Aminotransferases - blood c-Jun protein Caspase-3 Cecum Cecum - surgery Creatinine Creatinine - blood Cytokines Enzymes Febuxostat - therapeutic use Gelatinase Inflammation Injuries Interleukin-1beta - metabolism Interleukins JNK Mitogen-Activated Protein Kinases - metabolism JNK protein Kidney - drug effects Kidney - metabolism Kidney - pathology Kidneys Kinases Ligation Lipocalin Liver Liver - drug effects Liver - metabolism Liver - pathology Liver Diseases - drug therapy Liver Diseases - etiology Liver Diseases - metabolism Liver Diseases - pathology Male Malondialdehyde Nitric oxide Protective Agents - therapeutic use Proteins Rats, Wistar Reactive oxygen species Sepsis Sepsis - complications Sepsis - drug therapy Sepsis - metabolism Sepsis - pathology Signal transduction Superoxide dismutase Transcription factors Tumor necrosis factor-α Urea Urea - blood Uric acid Xanthine oxidase Xanthine Oxidase - metabolism |
| title | Protective effect of febuxostat in sepsis-induced liver and kidney injuries after cecal ligation and puncture with the impact of xanthine oxidase, interleukin 1β, and c-Jun N-terminal kinases |
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