【摘要】

目的 探讨白藜芦醇对血管性痴呆模型大鼠学习、记忆能力的影响及其可能机制。
方法 将40只雄性SD大鼠随机分为假手术组(sham)，模型对照组(VD-veh)，白藜芦醇低(VD-Res1)、高(VD-Res2)剂量治疗组。其中，VD-veh组及VD-Res治疗组应用2-VO法制作血管性痴呆大鼠模型；低、高剂量白藜芦醇治疗组分别给予白藜芦醇20 mg/(kg•d)、50 mg/(kg•d)腹腔注射14天；sham组及VD-veh组大鼠腹腔注射等量生理盐水。采用Morris水迷宫检测各组大鼠的学习记忆能力，并利用免疫印迹
方法检测各组大鼠脑组织tau蛋白与磷酸化tau(p-tau)的表达变化。
结果 与sham组相比，VD-veh组大鼠在Morris水迷宫测试中逃避潜伏期延长（P＜0.01），100s内穿越平台次数减少（P＜0.01）；白藜芦醇能够改善血管性痴呆大鼠的逃避潜伏期（P＜0.05）及穿越目标象限次数（P＜0.05）；与sham组相比，VD-veh组大鼠海马组织中p-tau表达显著升高（P＜0.05），而tau蛋白表达无明显差异（P>0.05），高剂量白藜芦醇干预可改善模型大鼠海马组织中p-tau的表达（P＜0.05）。
结论 白藜芦醇可能通过降低脑内磷酸化tau蛋白水平改善血管性痴呆模型大鼠的学习、记忆能力。

【Abstract】

Objective To investigate the effects of Resveratrol on learning and memory in rats with vascular dementia (VD) and the possible mechanism.
Methods 40 male SD rats were randomly divided into sham operation group (sham), model control group (VD-veh), low dose (VD-Res1) and high dose (VD-Res2) of Resveratrol treatment group. Rats in VD-veh group and VD-Res treatment groups were made to the model of vascular dementia rats useing 2-VO method . The low dose and high dose of resveratrol treated group were given resveratrol 20 mg/ (kg - D), 50 mg/ (kg - D) by intraperitoneal injection for 14 days; rats in the sham group and VD-veh group were injected with normal brine. Morris water maze was used to detect the learning and memory ability of rats in each group, the expression of tau protein and phosphorylated tau (p-tau) was detected by Western blots.
Results Compared to the sham group, rats in the VD-veh group had a increased escape latency in the Morris water maze (P < 0.01), and a decreased time of crossing platform (P < 0.01); Resveratrol can improve the studying ability (P < 0.05) and the times of passes through in the target quadrant (P < 0.05); compared to the sham group, VD-veh p-tau expression in hippocampus of rats was significantly increased (P < 0.05), the high dose of resveratrol intervention can reduce the p-tau in hippocampus of model rats (P < 0.05).
Conclusion   Resveratrol may improve the learning and memory ability of rats with vascular dementia by decreasing the level of phosphorylated tau protein in the brain.