Etanercept ameliorated renal Damage during Global Renal Ischemia-Reperfusion Injury in Male Rats

Background: The kidneys are injured by ischemia-reperfusion (IR), which causes inflammation and apoptosis, through the action of tumor necrosis factor (TNF)-alpha. In numerous studies that carried on renal damage. Etanercept has shown anti-inflammatory and anti-apoptotic characteristics. It is a soluble TNF-alpha receptor. The potential of etanercept to stop experimental renal IR injury was evaluated.Aims: The goal is to evaluate etanercept potential protection against widespread renal ischemia/reperfusion injury.Methods: Sprague-Dawley (SD) male rats were divided in to four groups: sham, DMSO-treated, etanercept-treated, DMSO-treated IR, and etanercept-treated IR groups. At 24 hours following an IR injury, ELIASA and IHC, respectively, were used to evaluate the renal levels of TNF-alpha and TLRS. Histopathological analysis was used to gauge the extent of renal cell injury.Results: After IR damage, IR rats treated with etanercept had significantly lower tissue levels of TNF-and TLRs than IR rats treated with DMSO. DMSO-treated IR rats had much higher levels of TNF-alpha and TLRs in their kidneys than DMSO-treated sham rats did, while etanercept-treated IR rats had significantly lower levels of TNF-alpha and TLRs than DMSO-treated IR rats did. Etanercept pre-treatment significantly reduced the damage score in IR-injured rats compared to the control and DMSO groups. Etanercept enhanced the downregulation of TLRs and TNF-via improving resistance to renal damage during IR.Conclusion: Renoproctive effect of Etanercept against renal I/R injury via down-regulation of TNF-alpha protein and inflammation.