8-Br-cADPR,a TRPM2 ion channel antagonist, inhibits renal ischemia-reperfusion injury
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Dosyalar
Tarih
2019
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Wiley
Erişim Hakkı
info:eu-repo/semantics/closedAccess
Özet
The 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.
Açıklama
Anahtar Kelimeler
8-Br-cADPR, cytokines, ischemia-reperfusion, oxidative stress, TRPM2, Cyclic-Adp-Ribose, Intracellular Free Calcium, Caspase-3 Gene-Expression, Oxidative Stress, Ischemia/Reperfusion Injury, Ryanodine Receptor, Molecular-Cloning, Oxidant Stress, Kidney Injury, Mice Lacking
Kaynak
Journal of Cellular Physiology
WoS Q Değeri
Q1
Scopus Q Değeri
Q1
Cilt
234
Sayı
4