Effect of Aerobic Exercise Combined with Anmeidan on Learning Memory and Synaptic Plasticity in Rats with Sleep Deprivation Based on BDNF/TrkB/CREB Signaling Pathway
10.13422/j.cnki.syfjx.20250618
- VernacularTitle:基于BDNF/TrkB/CREB信号通路探讨有氧运动联合安寐丹对睡眠剥夺大鼠学习记忆及突触可塑性的影响
- Author:
Yunyuan GUO
1
;
Yuping SHAO
2
;
Qiuchan ZENG
1
;
Lixia LIN
2
;
Guangjing XIE
3
Author Information
1. School of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan 430065, China
2. School of Physical and Health Education, Hubei University of Chinese Medicine, Wuhan 430065, China
3. Engineering Research Center of Traditional Chinese Medicine Protection Technology and New Product Development for the Elderly Brain Health, Ministry of Education, Hubei University of Chinese Medicine, Wuhan 430065, China
- Publication Type:Journal Article
- Keywords:
Anmeidan;
aerobic exercise;
sleep deprivation;
learning memory;
synaptic plasticity;
brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB)/ cAMP-response element binding protein (CERB)
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(17):117-124
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveThis paper aims to study the effects of four weeks of aerobic exercise combined with Anmeidan on the synaptic plasticity marker protein and synaptic ultrastructure of the hippocampus in the model rats with sleep deprivation, thereby investigating the possible mechanism of its action to improve the learning memory of rats with sleep deprivation. Methods50 Sprague-Dawley (SD) rats were randomly divided into blank control group (group C), sleep deprivation group (group M), aerobic exercise + sleep deprivation group (group MEX), Anmeidan + sleep deprivation group (group MA, 18.18 g∙kg-1∙d-1), and aerobic exercise + Anmeidan + sleep deprivation group (group MEXA, 18.18 g∙kg-1∙d-1). Anmeidan was administered by gavage in the MA group for four weeks. Aerobic exercise was performed in the MEX group for four weeks. Anmeidan was administered by gavage in the MEXA group in combination with aerobic exercise for four weeks, and sleep deprivation was performed for 72 h by using the multi-platform water environment method. At the end of sleep deprivation, Morris water maze was used to assess the learning and memory ability of rats in each group, and hematoxylin-eosin (HE) staining was used to observe the morphological changes of rats' hippocampal neurons. A transmission electron microscope was used to observe the synaptic ultrastructure of rats' hippocampus. The expression levels of brain-derived neurotrophic factor (BDNF), tyrosine kinase receptor B (TrkB), cAMP-response element binding protein (CREB), postsynaptic density-95 (PSD-95), and synaptophysin (SYN) were detected by Western blot, and the real-time fluorescence quantitative polymerase chain reaction (Real-time PCR) was used to detect the relative mRNA expression levels of BDNF, TrkB, and CREB in the rats' hippocampus. ResultsCompared with those in group C, rats in group M had significantly longer latency and total swimming distance on the platform (P<0.01) and a significantly reduced number of traversals across the platform as well as the residence time in the target quadrant (P<0.01). Part of the hippocampal neurons damaged, with a reduced number, disorganized arrangement, fuzzy synaptic gaps, thinning of post-synaptic dense material, and uneven density of synaptic vesicles. The protein expression levels and relative mRNA expression levels of BDNF, TrkB, and CREB were significantly reduced (P<0.01), and the protein expression levels of PSD-95 and SYN were significantly reduced (P<0.01). Compared with those in group M, rats in MA, MEX, and MEXA groups showed a decrease in latency to platform and total distance swum, an increase in the number of traversals across the platform and residence time in the target quadrant (P<0.05, P<0.01), a reduction in hippocampal neuronal damage, a better arrangement, a more intact synaptic structure, a thickening of post-synaptic dense material, a uniform density of synaptic vesicles, and an increase in the protein expression levels and mRNA expression levels of BDNF, TrkB, and CREB (P<0.05, P<0.01). The protein expressions of PSD-95 and SYN rose (P<0.05, P<0.01). ConclusionAerobic exercise combined with Anmeidan can improve learning memory in rats with sleep deprivation, and its mechanism of action may be related to the modulation of the BDNF/TrkB/CERB signalling pathway, up-regulation of the expression of PSD-95 and SYN, and improvement of synaptic structural damage. The combination of interventions is superior to single exercise or drugs.