title: The effect of quercetin on renal ischemia and reperfusion injury in the rat.
abstract: Renal ischemia-reperfusion injury occurs in many clinical conditions such as hypovolemic shock, thromboembolism, injury and after renal transplantation. Under these conditions, ROS are considered to be the reason for cellular damage. Bioflavonoids have antioxidant and renoprotective properties. We studied the effect of quercetin, a bioflavonoid, on ischemia and reperfusion in rats. The rats (n = 28) were separated into three groups. Group I was the control group. Animals in groups II (IR) and III (IR + Q) underwent 30 min ischemia and 45 min reperfusion, respectively. Rats, in group III, also received 50 mg kg(-1) quercetin before 45 min of reperfusion. The activities of SOD, CAT, GPx, and concentrations of GSH and GSSGR were determined in renal cortex and erythrocytes. Also, the levels of MDA in renal cortex and plasma, and XO in renal cortex were measured in these groups. The renal cortex XO levels in the IR group were higher than that of the control and IR+Q groups (p<0.001). The renal cortex and plasma MDA levels in the IR group were also found to be higher than the control and IR+Q groups (p<0.01, and p<0.001, respectively). However, a decrease in MAD level of the IR+Q group was found in renal cortex and erythrocytes. In addition, SOD, CAT, and GPx activities in renal cortex and erythrocytes of quercetin-treated animals were enhanced compared to animals of the IR group. Furthermore, there were no significant differences in the SOD, CAT, and GPx activities of the control and IR+Q group. A reduction of GSH and GSSGR levels in IR and IR+Q groups was detected but no significant differences were found between these groups. This study stresses that high concentration of ROS leads to renal ischemia and reperfusion, and quercetin reduces the renal injury by preventing the oxidative stress dependent on ischemia and reperfusion. Quercetin may be used in renal transplantation as an antioxidant drug.
authors.affiliation: Department of Biochemistry, The Medical School, Osmangazi University, Eskişehir-26480, Turkey.
authors.forename: Mine
authors.initials: M
authors.lastname: Inal
authors.forename: Mehmet
authors.initials: M
authors.lastname: Altinişik
authors.forename: Mehmet D
authors.initials: MD
authors.lastname: Bilgin
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002374:Catalase / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D007672:Kidney Cortex / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008956:Models, Chemical; D018384:Oxidative Stress; D011794:Quercetin / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D008315:Malondialdehyde; D011794:Quercetin; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione