Eraslan, ErsenTanyeli, AyhanPolat, ElifPolat, Elif2022-05-112022-05-1120190021-95411097-4652https://doi.org/10.1002/jcp.27236https://hdl.handle.net/20.500.11776/9200The transient receptor potential melastatin-2 (TRPM2) channel belongs to the transient receptor potential channel superfamily and is a cation channel permeable to Na+ and Ca (2+). The TRPM2 ion channel is expressed in the kidney and can be activated by various molecules such as hydrogen peroxide, calcium, and cyclic adenosine diphosphate (ADP)-ribose (cADPR) that are produced during acute kidney injury. In this study, we investigated the role of 8-bromo-cyclic ADP-ribose (8-Br-cADPR; a cADPR antagonist) in renal ischemia-reperfusion injury using biochemical and histopathological parameters. CD38, cADPR, tumor necrosis factor-, interleukin-1, and myeloperoxidase (inflammatory markers), urea and creatinine, hydrogen peroxide (oxidant), and catalase (antioxidant enzyme) levels that increase with ischemia-reperfusion injury decreased in the groups treated with 8-Br-cADPR. In addition, renin levels were elevated in the groups treated with 8-Br-cADPR. Histopathological examination revealed that 8-Br-cADPR reduced renal damage and the expression of caspase-3 and TRPM2. Our results suggest that the inhibition of TRPM2 ion channel may be a new treatment modality for ischemic acute kidney injury.en10.1002/jcp.27236info:eu-repo/semantics/closedAccess8-Br-cADPRcytokinesischemia-reperfusionoxidative stressTRPM2Cyclic-Adp-RiboseIntracellular Free CalciumCaspase-3 Gene-ExpressionOxidative StressIschemia/Reperfusion InjuryRyanodine ReceptorMolecular-CloningOxidant StressKidney InjuryMice LackingArticle234445724581Q1WOS:0004576137001182-s2.0-8505296036930191993Q1