香水莲花提取物对东莨菪碱诱导记忆障碍小鼠学习记忆能力的影响

探究香水莲花提取物(Nymphaea hybrid extract,NHE)对东莨菪碱诱导记忆障碍小鼠的学习记忆能力的影响。采用腹腔注射东莨菪碱建立记忆障碍模型,Morris水迷宫实验测定小鼠空间学习和记忆能力。水迷宫实验结束后,断头处死小鼠,进行生化指标的测定。结果表明,与模型组小鼠相比,NHE干预后,小鼠的逃避潜伏期明显缩短(P <0. 01),目标象限停留时间百分比和穿越平台次数增加(P <0. 05或P <0. 01),小鼠海马和皮质区的SOD和GSH-PX活力显著升高(P <0. 01或P <0. 05),MDA含量极显著降低(P <0. 01),ACh E活性显著降低(P <0. 01),ACh含量增加(P <0. 01或P <0. 05)。同时,免疫印迹结果表明,NHE能够改善东莨菪碱引起小鼠海马和皮质中ERK、CREB磷酸化水平和BDNF蛋白表达的减少。综上,香水莲花提取物可以提高东莨菪碱诱导的记忆障碍小鼠的学习记忆能力,具体机制涉及缓解大脑的氧化应激损伤,平衡胆碱能系统,激活ERK-CREB-BDNF信号通路。

Effect of Nymphaea hybrid extract on learning and memory ability of scopolamine-induced memory impaired mice

This research explored the effect of Nymphaea hybrid extract(NHE)on the learning and memory ability of scopolamine-induced memory impairment mice.The memory impairment model was established by intraperitoneal injection of scopolamine,and the spatial learning and memory ability of mice was determined by Morris water maze test.After the water maze experiment was completed,the mice were killed by decapitation and biochemical indicators were measured.The results showed that compared with the model group,after NHE intervention,the escape latency of the mice was significantly shortened(P<0.01),the target quadrant residence time percentage and the number of crossing platforms were increased(P<0.05 or P<0.01),the activity of SOD and GSH-PX in hippocampus and cortex of mice was significantly increased (P<0.01 or P<0.05),the content of MDA was significantly decreased (P<0.01),and the activity of AChE was significantly decreased (P<0.01),ACh content was increased(P<0.01 or P<0.05).At the same time,the results of immunoblotting showed that NHE could ameliorate the decrease of the phosphorylated ERK and CREB,as well as BDNF protein expression in hippocampus and cortex of mice induced by scopolamine.In summary,NHE could enhance the learning and memory ability of scopolamine-induced memory impairment mice.The specific mechanism involved alleviating oxidative stress damage in the brain,balancing the cholinergic system,and activating the ERK-CREB-BDNF signaling pathway.