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摘要
<jats:p> Arsenic trioxide (As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub>) is a known environmental toxicant and potent chemotherapeutic agent. Significant correlation has been reported between arsenic exposure (including consumption of arsenic-contaminated water and clinical use of As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub>) and dysfunction in the nervous system. In this study, we aimed to elucidate the effect of resveratrol with neuroprotective activities on As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub>-induced oxidative damage and cerebral cortex injury. Twenty-four healthy Chinese Dragon Li cats of either sex were randomly divided into four groups: control (1 ml/kg physiological saline), As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> (1 mg/kg), resveratrol (3 mg/kg) and As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> (1 mg/kg) + resveratrol (3 mg/kg). As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub>+resveratrol-treated group were given resveratrol (3 mg/kg) 1 h before As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> (1 mg/kg) administration. Pretreatment with resveratrol upregulated the activities of antioxidant enzymes and attenuated As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub>-induced increases in reactive oxygen species and malondialdehyde production. In addition, resveratrol attenuated the As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub>-induced reduction in the level of reduced glutathione and the ratio of reduced glutathione to oxidised glutathione, and accumulation of arsenic in the cerebral cortex. These findings support neuroprotective effect of resveratrol on As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub> toxicity in feline brain and provide a better understanding of the mechanism that resveratrol modulates As<jats:sub>2</jats:sub>O<jats:sub>3</jats:sub>-induced oxidative damage and a stronger rational for clinical use of resveratrol to protect brain against the toxicity of arsenic. </jats:p>
