脑损伤
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Figure 8｜Effect of exercise, and/or melatonin on pathological changes in hippocampal CA1 cells.
To determine the degree of synaptic plasticity associated with the above cognitive improvement, we observed cell morphology and synaptic structure in the CA1 region of the hippocampus. As shown in Figure 8, Nissl staining was used to observe the hippocampal CA1. The results showed that most neurons in the hippocampal CA1 of the MCAO group were lost, atrophied, or loosely arranged. Overall, the MCAO group had fewer hippocampal CA1 neurons than the Sham group (P < 0.05), and numbers of these neurons also differed between different treatment groups (P < 0.01). Pair-to-pair analysis showed that both exercise-only (P < 0.01) and exercise-with-melatonin therapy (P < 0.001) resulted in less hippocampal CA1 neural loss than was observed in the MCAO group. Additionally, the number of neurons in the combination therapy group did not differ from that in the Sham group.
Figure 9｜Effect of exercise, and/or melatonin on PSD thickness in the hippocampal CA1.
As shown in Figure 9, the PSD was significantly thinner after stroke (P < 0.05) and its thickness differed depending on the treatment (P < 0.01). Pair-to-pair analysis showed no significant differences between melatonin-only, exercise-only, and exercise-with-melatonin therapy (P > 0.05). Pathological changes in the hippocampal CA1 region indicate that combination therapy prevents cell death and improves synaptic plasticity.