缺血后处理对脑缺血大鼠学习记忆能力的影响

目的研究缺血后处理(IP)对大鼠脑缺血再灌注损伤后的学习和记忆能力的影响,探讨各组大鼠脑缺血再灌注后海马CA1区P淀粉样蛋白前体(APP)表达。方法将48只雄性SD大鼠随机分为3组:假手术组、对照组和缺血后处理组(IP组),每组16只大鼠。术后用Morris水迷宫方法测定大鼠认知记忆能力变化。3组大鼠脑组织切片行HE染色和APP染色,并行统计学分析。结果Morris水迷宫试验显示,对照组大鼠训练第1~4天逃避潜伏期长于IP组(P<0.01);跨越原平台次数IP组明显多于对照组(P<0.05)。HE染色结果显示,对照组大鼠海马CA1区神经元细胞脱失明显,而1P可减轻这种形态学改变。免疫组化结果显示,在脑缺血再灌注144h后对照组中APP表达明显高于假手术组(P<0.01);IP组海马CA1区APP表达较对照组减少(P<0.05)o结论缺血后处理可通过抑制APP的表达改善缺血再灌注后大鼠的记忆减退。

Effect of ischemic postconditioning on learning and memory in rats with cerebral ischemia

Objective To investigate the effect of ischemic postconditioning (IP) on learning and memory in rats after cerebral ischemia-reperfusion injury, and to investigate the expression of beta-amyloid precursor protein (APP) in the hippocampal CA1 region of rats after cerebral ischemia-reperfusion injury.Methods A total of 48 male Sprague-Dawley rats were equally and randomly divided into three groups:sham-operation group, control group, and IP group. Learning and memory ability of the rats was assessed with Morris water maze test before and after surgery. After the rats were sacrificed, brain tissue sections were prepared for HE staining and APP immunohistochemistry. A statistical analysis was performed on the data.Results The Morris water maze test showed that compared with the control group, the IP group had significantly shorter escape latency on 1-4 days of training and a significantly higher frequency of going through the original platform (P<0.01; P<0.05). HE staining showed that the neuronal cells in the hippocampal CA1 region of rats in the control group were significantly depleted and IP could alleviate the morphological change. Immunohistochemistry results suggested that compared with the control group, the sham-operation group had a significantly lower APP level in the hippocampal CA1 region at 144 hours after cerebral ischemia-reperfusion (P<0.01), and the IP group had a significantly reduced APP level (P<0.05).Conclusions Ischemic postconditioning can improve memory in rats after ischemia-reperfusion injury by inhibiting APP expression.