Objective: The aim: To investigate the Nephroprotective potential of Olmesartan in RIRI via modulation of the Nrf2/OH-1 signaling pathway.
Patients and methods: Materials and methods: Thirty male rats were equally divided into four groups. The sham group was exposed to surgical conditions without induction of RIRI. The control group was exposed to ischemia by clamping the renal pedicles for 30 min, followed by 2h of blood restoration. The vehicle-treated group was received dimethyl sulfoxide (DMSO) by intraperitoneal injection (IP) 30 min before clamping.
Results: Results: Olmesartan-treated group was pretreated with Olmesartan a dose of 10 mg/kg IP; 30 min prior to induction of ischemia. Following 30 min of ischemia, the clamps were released and allowed to the reperfusion for 2 h. Blood samples were collected to examine the levels of serum urea and creatinine. Kidney tissue was used to measure the levels of cytokines (TNFα, IL6, MCP, BAX, BCL2 and isoprostane F2. Immunohistochemistry was used to assess the levels of Nrf2 and HO-1. Histological analyses were used to detect the tubular damage in the kidney.
Conclusion: Conclusions: The results showed that Olmesartan alleviates renal tissue damage through activating the antioxidant effect mediated by Nrf2 signaling.
Keywords: Nrf2/HO-1 pathway; Olmesartan; apoptosis; inflammation; oxidative stress; renal ischemia reperfusion injury.