RESUMO
Background: Hyperuricemia (HU) is a metabolic disease characterized by high uric acid levels in the blood. HU is a risk factor for diabetes, cardiovascular complications, metabolic syndrome, and chronic kidney disease. Purpose: The present study was performed to determine the effect of experimental HU on xanthine oxidase (XO), tumor necrosis factor-alpha (TNF-α), nuclear factor-kappa B (NF-κB), interleukin-17 (IL-17), cytochrome C, glutathione peroxidase (GPx), caspase-3, and 8-hydroxydeoxyguanosine (8-OHdG) levels in liver tissues of rats. Study Design: Thirty-five, male, Wistar albino-type rats were used for this study. Experimental groups were formed as follows: Group 1: control group; Group 2: potassium oxonate (PO) group; group 3: PO+NAR (naringenin; 2 weeks) group; and Group 4: PO (2 weeks)+NAR (2 weeks) group (total of 4 weeks). Methods: The first group was not given anything other than normal rat food and drinking water. In the second group, a 250 mg/kg intraperitoneal dose of PO was administered for 2 weeks. In the third group, 250 mg/kg intraperitoneal PO (application for 2 weeks) and 100 mg/kg NAR intraperitoneally 1 hr after each application were administered. In the fourth group, intraperitoneal PO administration was applied for 2 weeks, followed by intraperitoneal administration of NAR for 2 weeks (4 weeks in total). At the end of the experimental period, XO, TNF-α, NF-κB, IL-17, cytochrome C, GPx, caspase-3, and 8-OHdG levels were determined in liver tissues. Results: HU increased XO, TNF-α, NF-κB, IL-17, cytochrome C, caspase-3, and 8-OHdG levels in liver tissues. However, both 2 and 4 weeks of NAR supplementation decreased these values, and also NAR supplementation led to an increase in GPx levels in tissues. Conclusions: The results of the study show that increased inflammation, apoptosis, and DNA damage in experimental HU can be prevented by administration of NAR due to inhibition of cytochrome C, NF-κB, caspase-3, and 8-OHdG.
Assuntos
Água Potável , Hiperuricemia , Masculino , Ratos , Animais , NF-kappa B/genética , NF-kappa B/metabolismo , NF-kappa B/farmacologia , Caspase 3/genética , Caspase 3/metabolismo , Caspase 3/farmacologia , Interleucina-17/genética , Interleucina-17/metabolismo , Interleucina-17/farmacologia , Fator de Necrose Tumoral alfa/metabolismo , Citocromos c/genética , Citocromos c/metabolismo , Citocromos c/farmacologia , 8-Hidroxi-2'-Desoxiguanosina , Xantina Oxidase/genética , Xantina Oxidase/metabolismo , Xantina Oxidase/farmacologia , Ácido Úrico , Glutationa Peroxidase/genética , Glutationa Peroxidase/metabolismo , Glutationa Peroxidase/farmacologia , Água Potável/efeitos adversos , Água Potável/metabolismo , Ratos Wistar , Apoptose , Inflamação/metabolismo , Fígado/metabolismo , Dano ao DNARESUMO
Ischemia-reperfusion leads to damage in cell or tissue due to insufficient blood flow. The aim of present study was to determine the effect of zinc, melatonin and zinc + melatonin supplementations during 3 weeks on muscle tissue and plasma MDA and GSH levels. This study was performed on 38 male Wistar-Albino rats. Experiments groups were designed as sham-control, ischemia-reperfusion (I/R), zinc + I/R, melatonin + I/R and zinc + melatonin + I/R Ischemia-reperfusion was induced by left femoral artery occlusion (1 hour) and reopening (1 hour). At the end of experiments tissue and blood samples were analysed for MDA and GSH. MDA levels were increased, GSH levels decreased in I/R groups. However, zinc and melatonin supplementation inhibited MDA and increased GSH levels in I/R groups. The results of present study show that increased lipid peroxidation in muscle tissue by ischemia-reperfusion may be prevented by zinc and melatonin or zinc plus melatonin supplementation.