The Effect of Quercetin on Oxidative Stress Parameters in A Fructose-Induced Experimental Metabolic Syndrome Model

Aim: With the rising prevalence of Metabolic Syndrome (MetS), antioxidant therapies for managing oxidative stress are gaining attention. Fructose, a major metabolic stressor and a prevalent sweetener in processed foods, plays a significant role in this condition. This study evaluates quercetin's effects on MetS components, specifically its ability to alleviate oxidative stress in liver tissue within a fructose-induced MetS model. Material and Methods: 24 Sprague-Dawley rats were randomly divided into four groups: control, fructose, quercetin, and fructose+quercetin. Quercetin (15 mg/kg/day) was administered via gavage, and a 20% fructose solution was provided in drinking water over 10 weeks. Key metabolic parameters, including body weight, blood pressure, serum glucose, triglycerides, insulin levels, and insulin resistance, were assessed to confirm MetS. Liver tissue was analyzed for oxidative stress markers, including malondialdehyde (MDA), advanced oxidation protein products (AOPP), nitric oxide (NO), total antioxidant status (TAS), total oxidant status (TOS), and the oxidative stress index (OSI). Results: Fructose administration successfully induced key metabolic syndrome components, such as obesity, hypertension, hypertriglyceridemia, hyperglycemia, and insulin resistance. Quercetin significantly reduced fructose-induced hypertension and insulin resistance, though its effects on obesity, hyperglycemia, and hypertriglyceridemia were limited. Fructose exposure markedly elevated liver MDA, AOPP, and TOS levels, with nonsignificant increases in NO and TAS. Co-administration of quercetin with fructose resulted in significantly higher MDA levels compared to controls, while AOPP levels were notably reduced. Conclusion: At the administered dose, quercetin showed limited efficacy in mitigating fructose-induced lipid peroxidation; however, it displayed notable antioxidant activity by modulating protein oxidation and NO levels. These findings provide valuable insights into the pathogenesis of metabolic syndrome and suggest potential therapeutic avenues for targeting its underlying components.