论文部分内容阅读
目的:观察白藜芦醇对实验性脑缺血大鼠海马神经元β淀粉样蛋白(Aβ42)和磷酸化Tau蛋白(pTau)表达影响及与学习记忆功能障碍的关系。方法:选取Wistar雄性成年大鼠96只,按随机数字表法分为假手术组、脑缺血组、白藜芦醇组。采用线拴法建立左侧大脑中动脉脑缺血大鼠模型。采用Morris水迷宫测试各组大鼠学习记忆能力;干湿重法测定脑组织含水量;免疫组织化学法检测Aβ42和p-Tau在海马CA1区的分布情况;Western Blot法检测Aβ42、Tau,p-Tau在海马CA1区的蛋白表达量。结果:脑缺血组较假手术组相比脑组织含水量增加,逃避潜伏期延长,穿越平台次数及平台象限停留时间均减少,并且海马CA1区Aβ42和p-Tau蛋白的表达显著上调,差异均有统计学意义(P<0.05)。白藜芦醇可显著减少脑组织含水量,改善学习和记忆功能障碍,下调海马CA1区Aβ42和p-Tau蛋白的表达,差异均有统计学意义(P<0.05)。结论:白藜芦醇可改善脑缺血大鼠脑水肿及学习记忆障碍,这种脑保护作用可能与下调海马CA1区Aβ42和p-Tau蛋白的表达相关。
AIM: To observe the effect of resveratrol on the expression of amyloid beta (Aβ42) and phosphorylated Tau protein (pTau) in hippocampal neurons and the relationship with learning and memory dysfunction in experimental cerebral ischemia rats. Methods: Ninety-six Wistar male adult rats were randomly divided into sham operation group, cerebral ischemia group and resveratrol group according to random number table. The model of left middle cerebral artery occlusion was established by tethering method. The Morris water maze was used to test the learning and memory abilities of rats in each group. The water content of brain tissue was measured by wet-dry method. The distribution of Aβ42 and p-Tau in hippocampal CA1 region was detected by immunohistochemical method. The expressions of Aβ42, Tau, p -Tau protein expression in hippocampal CA1 region. Results: Compared with the sham-operated group, the water content of cerebral ischemia group increased, the escape latency prolonged, the number of crossing the platform and the residence time in the platform quadrant decreased, and the expression of Aβ42 and p-Tau protein in hippocampal CA1 region were significantly increased There was statistical significance (P <0.05). Resveratrol can significantly reduce the water content of brain tissue, improve the learning and memory dysfunction, downregulate the expression of Aβ42 and p-Tau in hippocampal CA1 region, the differences were statistically significant (P <0.05). CONCLUSION: Resveratrol can improve cerebral edema and learning and memory impairment in rats with cerebral ischemia. This protective effect may be related to the down-regulation of the expression of Aβ42 and p-Tau protein in hippocampal CA1 region.