Hepatocurative potential of Thymoquinone against CCl4-Induced Hepatotoxicity: impact on antioxidant defense systems in rat liver and plasma
DOI:
https://doi.org/10.34188/bjaerv7n4-135Palavras-chave:
antioxidant, CCl4, hepatocurative, hepatotoxicity, oxidative stress markers and thymoquinoneResumo
This study evaluates the oxidative stress markers in a CCl4-induced hepatotoxicity model in rats and explores the hepatoprotective effects of Thymoquinone (TQ). The oxidative stress markers analyzed include Catalase (CAT) and Superoxide Dismutase (SOD) as enzyme markers, and Glutathione (GSH) and Malondialdehyde (MDA) as non-enzyme markers. These markers were assessed in both liver homogenate and plasma levels. CCl4 exposure significantly increased MDA levels, a marker of lipid peroxidation, and decreased GSH, reflecting severe oxidative stress and liver damage. Enzyme activities of CAT and SOD were also significantly reduced, indicating a weakened antioxidant defense system. This oxidative damage resulted from the generation of free radicals during CCl4 metabolism, causing liver cell membrane damage and disrupting homeostasis. Treatment with Thymoquinone showed a protective effect, particularly at a dose of 5 mg/kg/day, both prophylactically and curatively. TQ significantly restored CAT and SOD activity. However, GSH was only partially restored, with the higher TQ dose showing a greater impact than the lower dose. This study demonstrates that Thymoquinone offers hepatocurative effects by enhancing the activity of antioxidant enzymes. These results suggest that TQ could be a potential therapeutic agent for mitigating oxidative stress-related liver damage caused by CCl4.
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