Protective effect of N-(p-amylcinnamoyl) anthranilic acid, phospholipase A2 enzyme inhibitor, and transient receptor potential melastatin-2 channel blocker against renal ischemia-reperfusion injury

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dc.authoridTekin, Suat/0000-0002-2757-1802
dc.authoridCakir, Murat/0000-0002-2066-829X
dc.authoridTaşlidere, Aslı Cetin/0000-0003-3902-3210;
dc.authorwosidTekin, Suat/KEI-2266-2024
dc.authorwosidCakir, Murat/I-8643-2019
dc.authorwosidTaşlıdere, Aslı/ABI-8274-2020
dc.authorwosidTekin, Suat/AAG-1440-2021
dc.authorwosidTaşlidere, Aslı Cetin/AAB-3979-2021
dc.authorwosidTekin, Suat/IZD-9868-2023
dc.contributor.authorCakir, Murat
dc.contributor.authorTekin, Suat
dc.contributor.authorTaslidere, Asli
dc.contributor.authorCakan, Pinar
dc.contributor.authorDuzova, Halil
dc.contributor.authorGul, Cemile Ceren
dc.date.accessioned2024-08-04T20:45:26Z
dc.date.available2024-08-04T20:45:26Z
dc.date.issued2019
dc.departmentİnönü Üniversitesien_US
dc.description.abstractThe production of reactive oxygen species and inflammatory events are the underlying mechanisms of ischemia-reperfusion injury (IRI). It was determined that transient receptor potential melastatin-2 (TRPM2) channels and phospholipase A(2) (PLA(2)) enzymes were associated with inflammation and cell death. In this study, we investigated the effect of N-(p-amylcinnamoyl) anthranilic acid (ACA), a TRPM2 channel blocker, and PLA(2) enzyme inhibitor on renal IRI. A total of 36 male Sprague-Dawley rats were divided into four groups: control, ischemia-reperfusion (I/R), I/R + ACA 5 mg, I/R + ACA 25 mg. In I/R applied groups, the ischemia for 45 minutes and reperfusion for 24 hours were applied bilaterally to the kidneys. In the I/R group, serum levels of the blood urea nitrogen (BUN), creatinine, cystatin C (CysC), kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and interleukin-18 increased. On histopathological examination of renal tissue in the I/R group, the formation of glomerular and tubular damage was seen, and it was detected that there was an increase in the levels of malondialdehyde (MDA), caspase-3, total oxidant status (TOS), and oxidative stress index (OSI); and there was a decrease in total antioxidant capacity (TAC) and catalase enzyme activity. ACA administration reduced serum levels of BUN, creatinine, CysC, KIM-1, NGAL, interleukin-18. In the renal tissue, ACA administration reduced histopathological damage, levels of caspase-3, MDA, TOS, and OSI; and it increased the level of TAC and catalase enzyme activity. It has been shown with the histological and biochemical results in this study that ACA is protective against renal IRI.en_US
dc.description.sponsorshipDepartment of Scientific Research Projects of Bozok University [6602c-TF/17-83]en_US
dc.description.sponsorshipDepartment of Scientific Research Projects of Bozok University, Grant/Award Number: 6602c-TF/17-83en_US
dc.identifier.doi10.1002/jcb.27664
dc.identifier.endpage3832en_US
dc.identifier.issn0730-2312
dc.identifier.issn1097-4644
dc.identifier.issue3en_US
dc.identifier.pmid30259992en_US
dc.identifier.scopus2-s2.0-85054010248en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage3822en_US
dc.identifier.urihttps://doi.org/10.1002/jcb.27664
dc.identifier.urihttps://hdl.handle.net/11616/98478
dc.identifier.volume120en_US
dc.identifier.wosWOS:000458459600116en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Cellular Biochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectN-(p-amylcinnamoyl) anthranilic aciden_US
dc.subjectphospholipase A(2)en_US
dc.subjectrenal ischemia-reperfusion injuryen_US
dc.subjecttransient receptor potential melastatin-2 channelsen_US
dc.titleProtective effect of N-(p-amylcinnamoyl) anthranilic acid, phospholipase A2 enzyme inhibitor, and transient receptor potential melastatin-2 channel blocker against renal ischemia-reperfusion injuryen_US
dc.typeArticleen_US

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