Abstract
Purpose: To observe the effects of EA on the expression of PS1protein level inhippocampusof SAMP8mice. Investigating themechanismof EA in therapeutic intervention of Alzheimer Disease (AD). Methods: Ten male SAMR1 mice as the Normal control group. Twenty male SAMP8 mice were randomly divided into Model group and EA group (n=10 in each group). EAwas stimulated at Baihui (GV20) andYintang (GV29) for 20min once a day (2V, 1mA). After 15 days, learning and memorizing abilities of mice were detected through Morris water maze. Observe the morphologic changes of PS1 and related metabolites in hippocampus through immunohistochemistry. Detecting PS1 level in hippocampus through Western blot method. Results: 1) Each group showed a significant difference in latency time in different days. 2) Compared with normal control group, Model group showed an increasing latency time and a decreasing swimming time to passing through the platform and quadrants (P < 0.05, P < 0.01), while EA group showed an obvious decreasing latency time (P<0.05, P < 0.01) and an increasing swimming time (P<0.01). 3) Immunohistochemical detection showedmice in EA group had a significant reduction in the expression of PS1 level in hippocampuswhile compared with theModel group. 4) Findings ofWestern blot revealed that compared with Model group, mice in Normal control group and EA group both had a reduction of PS1 content in hippocampus (P<0.05). Conclusion: EA could have a certain effect to improve the learning andmemorizing abilities of SAMP8mice and, to some extent, may be able to help prevent AD. However, the regulating effect of EA on PS1 level is much greater, this outcome could be seen as one of the mechanisms of treating AD. Contact: Jin Cao, jade cao@yeah.net
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