Etanercept Mitigated Renal Injury in Male Rats Undergoing Global Renal Ischemia-Reperfusion

• Published in: Azerbaijan Pharmaceutical and Pharmacotherapy Journal Vol. 22; no. 1; pp. 13 - 17
• Main Authors: Abbas, Ashwaq Najemaldeen, Mahdi, Fatimah Mohammed Saeed, Abed, Aumaima Tariq, Hassan, Saif M
• Format: Journal Article
• Language: English
• Published: Baku Azerbaijan Medical University 2023
• Subjects: Apoptosis; Edema; General anesthesia; Inflammation; Ischemia; Kidney diseases; Kidney transplants; Mortality; Scanning electron microscopy; Tumor necrosis factor-TNF
• ISSN: 1994-1951
• DOI: 10.61336/appj/22-1-04

Introduction: The kidneys are vulnerable to injury from ischemia-reperfusion (IR), a process that triggers inflammation and apoptosis, primarily mediated by tumor necrosis factor (TNF)-alpha. Numerous studies have investigated renal damage in this context. Etanercept, a soluble receptor for TNF-alpha, has demonstrated anti-inflammatory and anti-apoptotic properties. This study aims to assess the potential of etanercept in mitigating experimental renal IR injury and its capacity to protect against widespread renal ischemia/reperfusion injury. Methods: Male Sprague-Dawley (SD) rats were classified into four groups: sham, DMSO-treated, etanercept-treated, DMSO-treated IR, and etanercept-treated IR groups. After 24 hours following IR injury, renal levels of TNF-alpha and TERs (Toll-like receptors) were assessed using EEISA and IHC methods, respectively. Histopathological analysis was employed to quantify the extent of renal cell injury. Results: Etanercept treatment significantly lowered tissue levels of TNF-alpha and TLRs in IR-damaged rats compared to DMSO-treated IR rats. Kidneys of DMSO-treated IR rats exhibited substantially elevated levels of TNF-alpha and TLRs when compared to DMSO-treated sham rats. Conversely, etanercept-treated IR rats displayed significantly reduced levels of TNF-alpha and TLRs compared to DMSO-treated IR rats. Pre-treatment with etanercept significantly alleviated the extent of damage in IR-injured rats compared to the control and DMSO groups. Etanercept further promoted the downregulation of TLRs and TNF-alpha, thereby enhancing resistance to renal damage during IR. Conclusion: In conclusion, etanercept shows promise in providing protection against renal ischemia-reperfusion injury by mitigating inflammation and apoptosis, as evidenced by reductions in TNF-alpha and TLR levels. This suggests its potential as a therapeutic intervention to mitigate renal damage resulting from ischemia-reperfusion injury.