8-Br-cADPR,a TRPM2 ion channel antagonist, inhibits renal ischemia-reperfusion injury


ERASLAN E. , TANYELİ A., Polat E., POLAT E.

JOURNAL OF CELLULAR PHYSIOLOGY, vol.234, no.4, pp.4572-4581, 2019 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 234 Issue: 4
  • Publication Date: 2019
  • Doi Number: 10.1002/jcp.27236
  • Title of Journal : JOURNAL OF CELLULAR PHYSIOLOGY
  • Page Numbers: pp.4572-4581

Abstract

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.