Dexmedetomidineprotects against ischemia and reperfusioninduced kidney injury in rats by inhibiting the expression of TRPM2 and TRPA1 channels

Abstract

Objective(s): Renal ischemia and reperfusion (I/R) injury is a potentially serious issue encountered during various medical and surgical procedures. This condition is clinically significant because of its high incidence and mortality rate. In this study, we aimed to investigate the protective effect of dexmedetomidine (DEX) on oxidative stress-activated TRPM2 and TRPA1 channel expression in rats with a renal I/R model. Materials and Methods: A total of 35 rats were used in the study. The animals were divided into five groups. The control group received no procedure during the experiment. In the sham group, the abdomen was opened under general anesthesia, the right kidney was removed, and the left renal pedicle was exposed; however, a renal clamp was not applied. The dexmedetomidine group received dexmedetomidine, using the same surgical procedure. In the I/R groups, rats were subjected to left renal ischemia for 30 min followed by 45 min of reperfusion. Dexmedetomidine was not administered to the I/R group, while dexmedetomidine was given to the I/R+DEX group at the beginning of reperfusion. TRPM2 and TRPA1 levels were analysed in serum and kidney tissues at the end of the experiment. Results: A significant increase in TRPM2 and TRPA1 expression was observed in all samples from the I/R group compared to the non-I/R groups, while a significant decrease in TRPM2 and TRPA1 expression was seen at the I/R+DEX compared to the I/R. Conclusion: Dexmedetomidine may have renoprotective effects in I/R injury by inhibiting redox-TRP channels.