Acute kidney injury (AKI) frequently occurs due to renal ischemia/reperfusion injury (IRI), which is marked by damaged tissue and a decrease in blood flow to the kidneys. IRI causes Oxidative damage, inflammation, and cell death. Autophagy, which recycles cytoplasmic components and breaks them down into smaller pieces, may have a role in cell death or survival in certain pathological states.
Objective: Through antioxidant, anti-inflammatory, and anti-apoptotic actions, as well as activation of the autophagy system, this study explores the potential nephroprotective benefits of trandolapril against renal ischemia-reperfusion damage. Material and method: There were four groups of rats used in this study: sham, RIRI, Dimethyl sulfoxide, and Trandolapril pretreated groups. The sham group underwent the same anesthesia and surgical procedures except for ischemia. Other groups undergo bilateral renal ischemia for 30 minutes and then reperfusion for 24 hours. DMSO group vehicle for trandolapril and trandolapril group 0.3mg/kg given 2 hours before ischemia induction. Results: The study found that blood urea and serum creatinine levels increased in the RIRI and DMSO groups when compared with the sham group. Renal tissue levels of IL-6, Kim-1, caspase-3, LC-3, and Akt were also elevated in RIRI while GSH levels decreased in the RIRI. The Trandolapril group showed significant increases in GSH, LC-3, and Akt levels when compared to the sham group. Trandolapril reduced serum urea and creatinine levels, and renal tissue levels of IL-6, Kim-1, and caspase-3 also reduced.
Conclusion: Male rat models of ischemia-reperfusion injury showed that trandolapril significantly decreased kidney damage.