{"title":"Moexipril Improves Renal Ischemia/Reperfusion Injury in Adult Male Rats","authors":"Esraa H. Alsaaty, Ali M. Janabi","doi":"10.22317/jcms.v10i1.1477","DOIUrl":null,"url":null,"abstract":"Objective: The goal of this study is to see if moexipril can protect rats against renal ischemia/reperfusion injury.\nMethods: Overall twenty-eight males of rats were divided randomly into four groups (7 rat each group). Sham group: Except for ischemiainduction, these rats underwent IP anesthesia and surgery. Induced group: This group rats were anesthetized and given a midlinelaparotomy to induce bilateral renal ischemia for 30 min and 2 hours of reperfusion. DMSO group: Rats received DMSO IP injection 30 minbefore ischemia and subjected to 30 min bilateral ischemia and reperfusion for 2 hours, DMSO is a vehicle of moexipril and considered ascontrol. Moexipril group (pretreated group): moexipril was given in a dose 0.3 mg/kg I.P. injection 30 min before ischemia.\nResults: Renal IRI as indicated by a significant increase (P < 0.05) in urea, creatinine, NF-KB P65, IL-1β, and caspase-3 level, while GSH,SOD, and Bcl-2 levels significantly (P < 0.05) reduced in Renal tissues of rats in the induced group compared to sham group. Moexiprilpretreatment significantly (P < 0.05) ameliorate RIRI as suggested from significant lowering in urea, creatinine, and inflammatory markers(NF-KB P65 and IL-1β). The renal level of oxidative marker (SOD and GSH) and anti-apoptotic marker Bcl-2 were significant decreased(P < 0.05) and also significantly increase (P < 0.05) in caspase-3 level with moexipril group in comparison to induced group.\nConclusion: By inhibiting oxidative stress, inflammation, and the apoptotic pathway, moexipril significantly protect from renal ischemiareperfusion in rats.","PeriodicalId":42860,"journal":{"name":"Journal of Contemporary Medical Sciences","volume":null,"pages":null},"PeriodicalIF":0.2000,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Contemporary Medical Sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22317/jcms.v10i1.1477","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: The goal of this study is to see if moexipril can protect rats against renal ischemia/reperfusion injury.
Methods: Overall twenty-eight males of rats were divided randomly into four groups (7 rat each group). Sham group: Except for ischemiainduction, these rats underwent IP anesthesia and surgery. Induced group: This group rats were anesthetized and given a midlinelaparotomy to induce bilateral renal ischemia for 30 min and 2 hours of reperfusion. DMSO group: Rats received DMSO IP injection 30 minbefore ischemia and subjected to 30 min bilateral ischemia and reperfusion for 2 hours, DMSO is a vehicle of moexipril and considered ascontrol. Moexipril group (pretreated group): moexipril was given in a dose 0.3 mg/kg I.P. injection 30 min before ischemia.
Results: Renal IRI as indicated by a significant increase (P < 0.05) in urea, creatinine, NF-KB P65, IL-1β, and caspase-3 level, while GSH,SOD, and Bcl-2 levels significantly (P < 0.05) reduced in Renal tissues of rats in the induced group compared to sham group. Moexiprilpretreatment significantly (P < 0.05) ameliorate RIRI as suggested from significant lowering in urea, creatinine, and inflammatory markers(NF-KB P65 and IL-1β). The renal level of oxidative marker (SOD and GSH) and anti-apoptotic marker Bcl-2 were significant decreased(P < 0.05) and also significantly increase (P < 0.05) in caspase-3 level with moexipril group in comparison to induced group.
Conclusion: By inhibiting oxidative stress, inflammation, and the apoptotic pathway, moexipril significantly protect from renal ischemiareperfusion in rats.