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Background and Aim: Propolis has a protective effect against cellular damage caused by toxic agents such as drugs, metals, xenobiotics, and chemicals. The aim of this study was to investigate the antioxidant activity and the effect of ethanolic extract of propolis on carbon tetrachloride (CCl4)-induced oxidative stress on kidney and liver injury in rat.Materials and Methods: The study quantified phenol, flavone, and flavonol in propolis and assessed antioxidant activity using 2, 2-diphenyl-1-picrylhydrazyl, ferric reducing antioxidant power, and molybdate. The investigators used four groups of rats to study the effect of propolis on CCl4-induced toxicity. Propolis extract was given orally (500 mg/kg) for 12 days, and CCl4 (1 mL/kg) was administered intraperitoneally on day 5 of the experiment. Blood and tissue samples of the liver and kidney were collected on day 13 to measure biochemical and oxidative parameters. The parameters included malondialdehyde (MDA), protein carbonyl formation (PCO), advanced oxidation protein products (AOPP), catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), and ascorbic acid (AA). Biochemical parameters included liver enzymes, blood urea (BU), creatinine, and uric acid (UA).Results: CCl4 decreased antioxidant agents, including CAT, GPx, GSH, and AA in the liver and kidney tissues. The oxidative agents' levels, including MDA, PCO, and AOPP, increased by CCl4 compared to the control group. CCl4 increased liver enzymes, UA, BU, and creatinine in the blood samples. Propolis significantly alleviated liver and kidney function, improved antioxidant parameters, and decreased levels of oxidative agents.Conclusion: The data showed for the 1st time that Moroccan propolis has a protective effect against CCl4-induced kidney and liver toxicity by maintaining the activity of the antioxidant defense system, which was most likely due to its antioxidant activity.

veterinary world/veterinary world

Antioxidant activity and protective effect of propolis against carbon tetrachloride-induced liver and kidney injury by modulation of oxidative parameters