MAS Receptor Agonist (AVE0991) Attenuate Renal Ischemia-Reperfusion Injury A Mouse Model

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Lafta F. Kadhim, Sarmad Nory Gany, Najah R. Hadi, Salim F. Kadhim


Renal ischemia/reperfusion injury (I/R) is a common cause of acute kidney injury (AKI) in patients, and renal blood stream obstruction is inevitable after renal transplantation. In the present study, we investigated the renal effects of acute administration of the Mas receptor agonist, AVE0991, in a murine model of AKI caused by reperfusion of ischemic kidneys. Mice were divided into four groups: control group, sham group, control vehicle group, and treatment of mice with AVE09. Histopathological analysis revealed an increase in tissue damage after IRI, as shown by the presence of vacuolization, dilated renal tubules, and glomerular alterations, as well as a dilatation of the Bowman's capsule and a lack of brush boundaries. Hematoxylin and eosin (H&E) staining revealed a decrease in the serum levels of interleukin-10 (IL-10), IL-6, and tumor necrosis factor-alpha (TNF-a). Treatment of mice, however, significantly improved renal injury (P 0.05) as compared to the control group and the overall severity score mean of this group revealed moderate renal impairment. The renoprotective effects of AVE 0991, when taken prior to renal I/R damage, were highly comparable to those induced by the AT1 receptor antagonist Losartan.

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