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Comparative Study
Journal Article
Protective effect of quercetin on renal ischemia/reperfusion injury in rats.
Journal of Nephrology 2003 March
BACKGROUND: 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. The aim of this study was to evaluate whether quercetin, an oxygen free radical scavenger, protects kidney tissue.
METHODS: A renal I/R injury was induced by a left renal pedicle occlusion by ischemia for 45 min, followed by 60 mins of reperfusion with contralateral nephrectomy in rats. The rats were pretreated intraperitoneally with a quercetin suspension (50 mg/kg) 60 min before the ischemia induction. Thiobarbituric acid reactive substances (TBARS), protein carbonyl content, tumor necrosis factor alpha (TNF-alpha), reduced glutathione (GSH) levels, myeloperoxidase (MPO) catalase (CAT) and superoxide dismutase (SOD) activities were determined in renal tissue.
RESULTS: There were 3 groups of rats, the control group, the I/R group and the I/R+Q group. Our results indicate that TBARS, TNF-alpha levels, MPO activity and protein carbonyl content were significantly higher in the I/R group than those in the control group (p<0.05, p<0.01, p<0.01 and p<0.01, respectively). Quercetin administration significantly decreased these parameters (p<0.05, p<0.01, p<0.05 and p<0.01, respectively). GSH levels, SOD, and CAT activities significantly decreased after I/R injury when compared to the control group (p<0.01, p<0.05 and p<0.01, respectively). Quercetin treatment significantly increased GSH levels and activities of these enzymes when compared to the I/R group (p<0.05, p<0.01, p<0.05, respectively).
CONCLUSIONS: These results suggest that quercetin reduces renal oxidative injury and facilitates repair. Quercetin can have a role in a renoprotective therapeutic regimen.
METHODS: A renal I/R injury was induced by a left renal pedicle occlusion by ischemia for 45 min, followed by 60 mins of reperfusion with contralateral nephrectomy in rats. The rats were pretreated intraperitoneally with a quercetin suspension (50 mg/kg) 60 min before the ischemia induction. Thiobarbituric acid reactive substances (TBARS), protein carbonyl content, tumor necrosis factor alpha (TNF-alpha), reduced glutathione (GSH) levels, myeloperoxidase (MPO) catalase (CAT) and superoxide dismutase (SOD) activities were determined in renal tissue.
RESULTS: There were 3 groups of rats, the control group, the I/R group and the I/R+Q group. Our results indicate that TBARS, TNF-alpha levels, MPO activity and protein carbonyl content were significantly higher in the I/R group than those in the control group (p<0.05, p<0.01, p<0.01 and p<0.01, respectively). Quercetin administration significantly decreased these parameters (p<0.05, p<0.01, p<0.05 and p<0.01, respectively). GSH levels, SOD, and CAT activities significantly decreased after I/R injury when compared to the control group (p<0.01, p<0.05 and p<0.01, respectively). Quercetin treatment significantly increased GSH levels and activities of these enzymes when compared to the I/R group (p<0.05, p<0.01, p<0.05, respectively).
CONCLUSIONS: These results suggest that quercetin reduces renal oxidative injury and facilitates repair. Quercetin can have a role in a renoprotective therapeutic regimen.
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