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The Mechanism of Aerobic Exercise Regulating the PI3K/Akt-mTOR Signaling Pathway Intervenes in Hippocampal Neuronal
Lei Gao1, Fushun Liu2, Ruilian Liu3
1Department of Physical Education, Yuzhang Normal University, Nanchang 330103, China.
Background:
The purpose of this paper is to explore the mechanism of aerobic exercise regulating autophagy through the PI3K/Akt-mTOR signaling pathway and its participation in apoptosis, to protect the hippocampal nerves from damage in vascular dementia rats.
Methods:
Thirty-six healthy male SD rats were randomly divided into a sham group, a model group, and a model exercise group. A neurobehavioral assessment was used to determine the memory and exploration abilities of the rats. A TUNEL assay was used to detect hippocampal neuron apoptosis. Immunohistochemical and Western blot analyses were used to analyze LC3Ⅱ and the beclin-1 protein. An RT-PCR detected the differential expression of mRNA.
Results:
The results of the neurobehavioral tests showed that the platform latency time of the rats with vascular dementia was prolonged. Aerobic exercise significantly shortens the swimming time of rats in platform latency. The TUNEL results showed that the TUNEL-positive cells of the hippocampal neurons in the model group increased; the expression of pro-apoptotic genes caspase-3 and Bax mRNA was up-regulated, and the expression of Bcl-2 mRNA was down-regulated. Aerobic exercise reduced hippocampal neuronal apoptosis, up-regulated Bcl-2 mRNA, and down-regulated caspase-3 and Bax mRNA. The LC3Ⅱ and Beclin-1 proteins, detected by immunohistochemistry and a Western blot analysis, showed that the protein expression in the hippocampi of rats with vascular dementia increased. Aerobic exercise reduced LC3Ⅱ and Beclin-1 protein expression. The results of the RT-PCR showed similar changes.
Conclusions:
Aerobic exercise could improve the learning and memory abilities of vascular dementia rats, moderately regulate the process of autophagy, reduce the TUNEL-positive cells of hippocampal neurons, repair damaged hippocampal neurons by regulating the autophagy signaling pathway PI3K/Akt-mTOR, and improve hippocampal function.
