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Abstract
There is increasing evidence to suggest that toxic oxygen radicals play a role in
the pathogenesis of ischemia/reperfusion (I/R) injury in the kidney. This study was
designed to investigate the effects of trimetazidine, in I/R induced renal failure
in rats. The protective effect of trimetazidine (Tmz) against the damage inflicted
by reactive oxygen species (ROS) during renal I/R was investigated in Sprague-Dawley
rats using histopathological and biochemical parameters. In one set of experiments
animals were unilaterally nephrectomized, and subjected to 45 min of left renal pedicle
occlusion and in another set both the renal pedicles were occluded for 45 min followed
by 24 h of reperfusion. Trimetazidine (3 mg kg(-1), i.p.) was administered 30 min
prior to ischemia and repeated 12 h after the first dose. At the end of the reperfusion
period, rats were sacrificed. Thiobarbituric acid reactive substances (TBARS), reduced
glutathione (GSH) levels, glutathione reductase (GR) catalase (CAT), and superoxide
dismutase (SOD) activities were determined in renal tissue. Serum creatinine and blood
urea nitrogen (BUN) concentrations were measured for the evaluation of renal function.
Ischemic control animals demonstrated severe deterioration of renal function, renal
morphology and a significant renal oxidative stress. Pretreatment of animals with
trimetazidine markedly attenuated renal dysfunction, morphological alterations, reduced
elevated TBARS levels and restored the depleted renal antioxidant enzymes. The findings
imply that ROS play a causal role in I/R induced renal injury and trimetazidine exert
renoprotective effects probably by the radical scavenging and antioxidant activities.