白藜芦醇对C57BL/6J 小鼠高热量饮食所致学习记忆障碍的预防作用
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Resveratrol prevents high-calorie diet-induced learning and memory dysfunction in juvenile C57BL/6J mice
背景
白藜芦醇已被证明可以改善学习和记忆,所以我们研究了白藜芦醇对饲喂高脂饮食的幼鼠学习记忆障碍的潜在影响,并探索这个过程所包含的分子机制。
方 法
6周龄(C57BL/6J)小鼠随机分为三组:对照组,HC饮食组,HC+RSV饮食组。用酶联免疫吸附实验测定血清胰岛素和胰岛素样生长因子水平,蛋白表达有免疫组化和蛋白印迹法测定。
结 果
每日给药RSV30mg/kg可防止高脂饮食导致的幼体体重增加,但并没有改变其他任何生理指标,包括,空腹血糖,血清胆固醇,甘油三酯,胰岛素及胰岛素样生长因子水平,且在HC组,RSV的确改善了学习记忆障碍。不管是在HC组还是HC+RSV组,过氧化物酶增值物激活受体r在海马CA1区下调了,但在HC+RSV组更显著。HC组的P16神经元数量减少了,HC+RSV组的海马CA1区P16表达水平与HC组比较明显上调了。
结 论
RSV能预防高脂饮食喂养的幼年动物学习记忆障碍,可能通过上调海马CA1区的P16或下调PPARy.
原始文献摘要
Objective
Because resveratrol (RSV) has been shown to improve learning and memory, so we investigated the potential benefit of RSV on learning and memory deficits in juvenile mice fed with a HC diet and explored the molecular mechanisms underlying this process.
Methods
Six-week-old C57BL/6J mice were divided into three different diet groups: control,HC diet, and HC + RSV diet. Serum insulin and insulin-like growth factor 1 (IGF-1) levels were measured using enzyme-linked immunosorbent assays. Protein expression was examined by immunohistochemistry and western blotting.
Results
Administration of RSV daily (30 mg/kg) prevented the HC diet-induced increase in juvenile animal body weight but did not improve any other physiological conditions, including
fasting blood glucose and serum cholesterol, triglyceride, insulin, and IGF-1 levels.However, RSV did prevent learning and memory deficits in the HC group.Peroxisome proliferator-activated receptor gamma (PPARγ) was downregulated in the CA1 region of the hippocampus in both the HC and HC + RSV groups, but the reduction was significantly
greater in the HC + RSV group (P < .01 compared with the HC group). Moreover, although the HC diet reduced the number of p16-positive neurons, the HC + RSV diet significantly
upregulated p16 expression in the CA1 region of the hippocampus (P < .01 compared with the HC group).
Conclusions
RSV protected against learning and memory impairments in juvenile animals fed with a HC diet, possibly via upregulation of p16 or downregulation of PPARγ in the hippocampal CA1 region.

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