Prevention of renal ischemia/perfusion-induced renal and hepatic injury in adult male Albino rats by oxytocin: role of nitric oxide.

BACKGROUND: Oxytocin (OT) has an anti-inflammatory and antioxidant effect in the different inflammatory models. The current study aimed to evaluate the protective function of OT in renal and hepatic damages triggered by renal ischemia/reperfusion (IR) in rats. Moreover, the effect of NG-nitro-l-arginine methyl ester (l-NAME) was investigated on the kidney and liver functions in renal IR model.

METHODS: Twenty-four rats were divided into four groups (six rats each) as follows: (1) Sham-operated group; (2) Renal IR group; (3) Renal IR+OT group; (4) Renal IR+OT+l-NAME. OT (1 mg/kg, i.p.) was administered 30 min prior to the induced ischemia and was repeated immediately before the reperfusion period. l-NAME (10 mg/kg, i.p.) was given 45 min before IR injury.

RESULTS: The results revealed that OT significantly attenuated the IR-induced elevations in the serum urea, creatinine, liver transaminases, and TNF-α levels, while nitric oxide (NO) and Bcl-2 levels were significantly increased compared with the IR group. OT also significantly compensated the decrease in the total antioxidant capacities (TAC) and lowered the elevated malondialdehyde (MDA) levels that were observed with renal IR in the renal and hepatic tissues.

CONCLUSIONS: In conclusion, OT ameliorates renal and hepatic damages triggered by renal IR, and this defense involves the suppression of inflammation and apoptosis with regulation of oxidant-antioxidant status. In addition, administration of l-NAME prior to OT partially reversed the protective effect of OT ensuring that one of the protective effects of OT was through the NO production.