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该实验利用APP/PS1双转基因模型小鼠,观察葛根素对小鼠学习记忆能力及tau蛋白磷酸化的影响。选用APP/PS1双转基因模型小鼠,3个月龄后开始灌胃给药。给药3个月后,通过Morris水迷宫实验测试小鼠学习记忆能力的变化;行为学测试结束后,处死动物,留取脑组织标本,ELISA法检测皮层Aβ水平;Western blot法检测皮层tau蛋白、磷酸化tau蛋白、GSK3β及磷酸化GSK3β(Ser9)蛋白表达情况。Morris水迷宫实验显示,APP/PS1双转基因模型小鼠逃避潜伏期较正常对照组明显延长,原象限停留时间明显缩短。葛根素组小鼠逃避潜伏期较模型组明显缩短,原象限停留时间明显延长。与正常对照组比较APP/PS1双转基因模型小鼠皮层Aβ水平增多,磷酸化tau蛋白表达显著增加,磷酸化GSK3β(Ser9)蛋白表达降低;给予葛根素后,APP/PS1转基因小鼠寻台潜伏期明显缩短,Aβ水平减少,磷酸化tau蛋白表达显著减少,磷酸化GSK3β(Ser9)蛋白表达增加。葛根素通过减少Aβ的生成,激活GSK3β信号通路,抑制tau蛋白磷酸化,改善APP/PS1双转基因模型小鼠的学习记忆损害。
In this experiment, APP / PS1 double transgenic mice were used to observe the effect of puerarin on learning and memory ability and phosphorylation of tau in mice. Selection APP / PS1 double transgenic mice, 3 months after the start of gavage. After 3 months of administration, the changes of learning and memory abilities of mice were tested by Morris water maze test. After behavioral test, animals were sacrificed and brain tissue samples were taken for the detection of cortical Aβ level by ELISA. Western blot was used to detect tau protein , Phosphorylated tau protein, GSK3β and phosphorylated GSK3β (Ser9) protein expression. Morris water maze test showed that APP / PS1 double transgenic mouse escape latency was significantly longer than the normal control group, the original quadrant of the residence time was significantly shorter. The puerarin group evacuation latency was significantly shorter than the model group, the original quadrant residence time was significantly prolonged. Compared with the normal control group, APP / PS1 double transgenic mouse model showed increased levels of Aβ, increased expression of phosphorylated tau protein and decreased expression of phosphorylated GSK3β (Ser9) protein in APP / PS1 transgenic mice. After administration of puerarin, Significantly shortened, decreased Aβ levels, phosphorylated tau protein expression was significantly reduced, phosphorylated GSK3β (Ser9) protein expression increased. Puerarin can ameliorate learning and memory impairments in APP / PS1 double transgenic mice by decreasing the production of Aβ, activating the GSK3β signaling pathway, inhibiting tau phosphorylation.