PROTECTIVE EFFECT OF EPROSARTAN IN RENAL ISCHEMIA REPERFUSION INJURY BY REGULATING OXIDATIVE STRESS, INFLAMMATION, AND APOPTOTIC CASCADES IN A BILATERAL RAT MODEL.

Abstract

The aim: To evaluate the potential protective effect of Eprosartan (ARB) in bilateral renal IRI in male rats. Materials and methods: 20 Sprague-Dawley rats divided into four groups. Sham group had surgery without IRI. Control group was subjected to 30 min ischemia and 2 hours of reperfusion. Vehicle group received 14 ml/kg (IP) injection of solvent mixture containing (10% DMSO, 40% PEG300, 5% Tween-80, and 45% normal saline) 30 minutes before clamping. Eprosartan-treated group with 30 mg/kg Eprosartan intraperitoneally 30 min before occlusion of renal pedicles followed by 30 minutes of ischemia and 2 hours of reperfusion. Serum BUN and Creatinine used to assess renal function. Renal tissue was used to measure the levels of TNF-α, IL-1β, IL-6, F2-isoprostane, and Caspase3 were measured by assessment of renal tissue. Histopathological examinations were conducted to detect parenchymal damage. Results: Mean serum levels of BUN and Creatinine as well as mean renal tissue levels of TNF-α, IL-1β, IL-6, F2-isoprostane, and Caspase3 were significantly increased in control and vehicle groups together with increase in histological damage score compared to sham group, whereas treatment of rats with Eprosartan resulted in significant reduction in mean serum levels of BUN and Creatinine and mean renal tissue levels of TNF-α, IL-1β, IL-6, F2-isoprostane, and Caspase3 and obvious reduction in tissue injury. Conclusions: This study demonstrates that Eprosartan pretreatment enhances kidney function by decreasing serum BUN and Creatinine, oxidative stress, cytokines, and apoptotic markers.