Protective Effect of Transient Receptor Potential Ankyrin 1 Inhibition on Renal Ischemia Reperfusion Injury in Rats

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dc.contributor.authorCakir, Murat
dc.contributor.authorAydin, Ali
dc.contributor.authorFirat, Semanur
dc.contributor.authorSekerci, Guldeniz
dc.contributor.authorBircan, Burak
dc.contributor.authorOz, Samet
dc.date.accessioned2026-04-04T13:37:39Z
dc.date.available2026-04-04T13:37:39Z
dc.date.issued2025
dc.departmentİnönü Üniversitesi
dc.description.abstractThe transient receptor potential ankyrin 1 (TRPA1) channels, characterized as nonselective cation channels with permeability to calcium ions (Ca2 +), are part of the extensive family of transient receptor potential (TRP) channels. Research has demonstrated that TRPA1 channels function as sensors for oxidative stress in the renal tubules. Additionally, TRPA1 expression has increased in renal tissue following ischemia-reperfusion (IR). There is also a significant correlation between IR-induced renal injury and TRPA1 expression. This study investigated the effects of selective TRPA1 agonist ASP7663 and selective TRPA1 antagonist HC-030031 on renal IR injury. A total of 40 rats were divided into four groups: control, IR, IR+ASP7663, and IR + HC-030031. The rat kidneys were exposed to 45 min of ischemia, followed by 24 h of reperfusion. TRPA1 agonist ASP7663 and selective TRPA1 antagonist HC-030031 were administered intraperitoneally to the treatment groups with renal IR. HC-030031 administration reduced the elevated kidney injury molecule-1 (KIM-1), blood urea nitrogen (BUN), and creatinine (Cre) caused by renal IR. HC-030031 administration reduced the increased histopathological damage in renal tissue due to IR. It also reduced renal tissue interleukin-1beta (IL-1 beta), interleukin-6 (IL-6), toll-like receptor-4 (TLR-4), phosphorylated-NF-kappa B, phosphorylated-I kappa B-alpha, tumor necrosis factor-alpha (TNF-alpha), and caspase-3 levels. In this study, TRPA1 antagonist HC-030031 showed a protective behavior on renal IR injury by averting inflammation and apoptosis. After further studies, TRPA1 inhibition may be a new treatment strategy to prevent renal IR injury.
dc.description.sponsorshipYozgat Bozok University Scientific Research Projects Unit [TD-2023-1097]
dc.description.sponsorshipThis study was financed by Yozgat Bozok University Scientific Research Projects Unit. (Project no: TCD-2023-1097).
dc.identifier.doi10.1002/jbt.70132
dc.identifier.issn1095-6670
dc.identifier.issn1099-0461
dc.identifier.issue1
dc.identifier.orcid0000-0002-2066-829X
dc.identifier.pmid39776031
dc.identifier.scopus2-s2.0-85214480245
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1002/jbt.70132
dc.identifier.urihttps://hdl.handle.net/11616/109968
dc.identifier.volume39
dc.identifier.wosWOS:001391185800001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Biochemical and Molecular Toxicology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WOS_20250329
dc.subjectASP7663
dc.subjectHC-030031
dc.subjectischemia-reperfusion
dc.subjectkidney
dc.subjecttransient receptor potential ankyrin 1 (TRPA1) channel
dc.titleProtective Effect of Transient Receptor Potential Ankyrin 1 Inhibition on Renal Ischemia Reperfusion Injury in Rats
dc.typeArticle

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