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姜黄素大鼠炎症实验灌胃

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Acrylonitrile (AN) is widely used in the manufacturing of fibers, plastics and pharmaceuticals. Free radicalmediated
lipid peroxidation is implicated in the toxicity of AN. The present study was designed to examine
the ability of curcumin, a natural polyphenolic compound, to attenuate acute AN-induced lipid peroxidation
in the brain and liver of rats. Male Sprague–Dawley rats were orally administered curcumin at
doses of 0 (olive oil control), 50 or 100 mg/kg bodyweight daily for 7 consecutive days. Two hours after
the last dose of curcumin, rats received an intraperitoneal injection of 50mg AN/kg bodyweight. Acute
exposure to AN significantly increased the generation of lipid peroxidation products, reflected by high
levels of malondialdehyde (MDA) both in the brain and liver. These increases were accompanied by a
significant decrease in reduced glutathione (GSH) content and a significant reduction in catalase (CAT)
activity in the same tissues. No consistent changes in superoxide dismutase (SOD) activity were observed
between the control and AN-treatment groups in both tissues. Pretreatment with curcumin reversed the
AN-induced effects, reducing the levels of MDA and enhancing CAT activity and increasing reduced GSH
content both in the brain and liver. Furthermore, curcumin effectively prevented AN-induced decrease in
cytochrome c oxidase activity in both liver and brain. These results establish that curcumin pretreatment
has a beneficial role in mitigating AN-induced oxidative stress both in the brains and livers of exposed
rats and these effects are mediated independently of cytochrome P450 2E1 inhibition. Accordingly, curcumin
should be considered as a potential safe and effective approach in attenuating the adverse effects
produced by AN-related toxicants.

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