Improvement Effect of Piceatannol on Cognitive Function of Mice with Alzheimer's Disease(白皮杉醇对阿尔茨海默病小鼠认知功能的改善作用)
摘要
To evaluate the improvement effect of piceatannol on cognitive impairment in Alzheimer's disease (AD) mice, seventy-two male Kunming mice were randomly divided into 6 groups with 12 mice in each group, including control group, model control group, positive control group, piceatannol intervention groups (low-dose, medium-dose and high-dose). AD mice were induced by AlCl<sub>3</sub> and D-galactose intervention for 70 d. After 5 weeks of continuous intervention with piceatannol on the 35th day of modeling, Morris water maze experiment was used to test the spatial learning and memory ability of mice. Meanwhile, the protein expression levels of Aβ1-42 and TNF-α in the hippocampus of mice were determined by ELISA method, and the activity of superoxide dismutase (SOD) and content of glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in mice serum were detected. Combined with relative viscera index, the improvement effect of piceatannol on AD mice was analyzed. The results showed that the latency of escape in model control group was significantly higher than that in control group and the memory ability was significantly decreased, while piceatannol effectively improved the cognitive behavior and memory ability of AD model mice (P<0.01). Compared with control group, the levels of Aβ1-42, TNF-α and activated microglia were significantly increased in model control group, while piceatannol significantly decreased the levels of Aβ1-42, TNF-α and activated microglia (P<0.01). Moreover, piceatannol effectively increased the activities of SOD and the content of GSH-Px and reduced MDA content in mice serum, and alleviated oxidative injury. In conclusion, piceatannol can improve the cognitive function of AD mice by reducing oxidative stress, neuroinflammation and Aβ production in the hippocampus.(研究白皮杉醇对阿尔茨海默病(Alzheimer's disease, AD)小鼠认知障碍的改善作用。取72只雄性昆明小鼠,随机分为6组,每组12只,即正常对照组、模型对照组、阳性对照组、白皮杉醇低、中、高剂量干预组。采用AlCl<sub>3</sub>和D-半乳糖联合诱导的方法连续干预70d,建立阿尔茨海默病小鼠模型。在造模35d开始用白皮杉醇连续干预,5