| Effect of Acupuncture and Moxibustion on Learning and Memory Ability and Main Pathological Features of SAMP8 Mice |
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| DOI： |
| EN KeyWords: Alzheimer’s disease acupuncture and moxibustion senescence-accelerated mouse-prone 8 learning and memory ability |
| Fund Project:国家自然科学基金面上项目（81873380；82074566） |
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| PDF Download Counts: 5591 |
| EN Abstract: |
| Objective：To explore the effects of acupuncture at GV20, HT7, and BL23 on the behavior, expression of β amyloid protein 1-42 (Aβ1-42), Tau protein and neuronal nuclei (NeuN) in hippocampus of SAMP8 mice. Methods：Six-month-old male SAMP8 mice were randomly divided into model group (n=6) and acupuncture treatment group (n=6), and SAMR1 male mice served as control group (n=6). Acupuncture treatment group was acupunctured at GV20 and HT7, then subjected to moxibustion on both sides of BL23 for 28 days. Morris water maze was used to evaluate the learning and memory ability of animals. The expression of Aβ1-42 and NeuN was detected by immunohistochemistry. Western blotting was used to detect the level of Tau protein in the hippocampus of mice. Results：As compared with the control group, escape latency was significantly prolonged (P<0.01), the residence time in the original platform quadrant was shortened (P<0.01), the number of crossing platforms was decreased (P<0.01), and the expression of Aβ1-42 was up-regulated (P<0.01), the expression of NeuN down-regulated (P<0.01), and the relative expression of hippocampal Tau protein up-regulating (P<0.01) in the model group. As compared with the model group at the second day, escape latency was shortened (P<0.01), the original platform quadrant stay time prolonged (P<0.05), the number of crossing platforms increased (P<0.05), the expression of hippocampal Aβ1-42 down-regulated (P<0.01), the expression of NeuN up-regulated (P<0.05) and the relative expression of hippocampal Tau protein down-regulated in the acupuncture treatment group. Conclusion：Acupuncture at GV20, HT7, and BL23 points can improve the learning and memory abilities of SAMP8 mice probably by reducing Aβ1-42 deposition and Tau protein levels, and inhibiting the decrease in the number of neurons. |
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