Prazosin Treatment Protects Brain and Heart by Diminishing Oxidative Stress and Apoptotic Pathways After Renal Ischemia Reperfusion

Acute kidney injury (AKI) is a major medical challenge caused from renal ischemia-reperfusion (IR) injury connected with different cellular events in other distant organs. Renal IR-related oxidative stress and inflammation followed by cell apoptosis play a crucial role in IR-induced distant organ pathological damages. Prazosin has shown protective effects against IR-injuries. Thus, the current study intended to investigate the possible protective role of prazosin against the consequents of renal IR in the heart and brain tissues. To reach this goal, rats were randomly divided into 3 groups (n = 7): Sham, IR and prazosin pretreatment-IR animals (1 mg/kg intraperitoneally injection of prazosin 45 min before IR induction). After 6 h reperfusion, lipid peroxidation and antioxidant markers levels were evaluated in the both, brain and hearttissue. Moreover, apoptotic pathway in the heart and brain tissues were assessed by western blotting. Accordingly, prazosin pretreatment in IR model rats could significantly increase the antioxidant capacity and attenuate apoptotic pathways by increasing the bcl-2 levels and decreasing the expression of Bax and caspase 3 enzymes (P<0.05). Thus, prazosin suppressed cellular damages of heart and brain tissues post kidney IR by anti-oxidative and anti-apoptotic effects, which suggests the plausible use of prazosin in improving the clinical outcomes during AKI after further investigations.