Department of Physical Education, Yuzhang Normal University, Nanchang 330103, China.
Police Sports Department, Zhejiang Police College, Hangzhou 310053, China.
Int J Environ Res Public Health. 2023 Jan 19;20(3):1893. doi: 10.3390/ijerph20031893.
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.
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.
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.
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.
本文旨在探讨有氧运动通过 PI3K/Akt-mTOR 信号通路调节自噬及其参与细胞凋亡，从而保护血管性痴呆大鼠海马神经免受损伤的机制。
将 36 只健康雄性 SD 大鼠随机分为假手术组、模型组和模型运动组。采用神经行为学评估检测大鼠的记忆和探索能力。TUNEL 法检测海马神经元凋亡。免疫组化和 Western blot 分析检测 LC3Ⅱ和 beclin-1 蛋白。RT-PCR 检测 mRNA 的差异表达。
神经行为学测试结果显示，血管性痴呆大鼠的平台潜伏期延长。有氧运动显著缩短血管性痴呆大鼠的游泳潜伏期时间。TUNEL 结果显示，模型组海马神经元的 TUNEL 阳性细胞增多；促凋亡基因 caspase-3 和 Bax mRNA 的表达上调，Bcl-2 mRNA 的表达下调。有氧运动减少海马神经元凋亡，上调 Bcl-2 mRNA，下调 caspase-3 和 Bax mRNA。免疫组化和 Western blot 分析检测到的 LC3Ⅱ和 Beclin-1 蛋白显示，血管性痴呆大鼠海马区的蛋白表达增加。有氧运动降低了 LC3Ⅱ和 Beclin-1 蛋白的表达。RT-PCR 结果也显示出相似的变化。
有氧运动可以改善血管性痴呆大鼠的学习记忆能力，适度调节自噬过程，减少海马神经元 TUNEL 阳性细胞，通过调节自噬信号通路 PI3K/Akt-mTOR 修复受损的海马神经元，改善海马功能。
