8周高强度间歇训练干预SIRT1/PGC1α通路对肥胖大鼠海马神经元损伤和认知功能障碍的影响

IF 3.2 Q2 NUTRITION & DIETETICS

Current Developments in Nutrition Pub Date : 2025-10-01 DOI:10.1016/j.cdnut.2025.107548

Kaiyin Cui , Jiabao Zhang , Huiting Wei , Yifu Meng , Changshuo Li , Ruizhe Liao , Jiajie Miao , Hao Su

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引用次数: 0

摘要

背景肥胖可引起认知功能的改变，导致认知障碍（CI）。目的探讨高强度间歇训练（HIIT）对肥胖大鼠海马神经元损伤、认知功能及SIRT1/PGC1α通路的影响，为HIIT干预改善肥胖所致CI提供理论依据。方法将肥胖造模成功的大鼠和同龄大鼠随机分为正常安静组（CSG, n = 10）、规律运动组（CEG, n = 10）、高脂安静组（HSG, n = 10）和高脂运动组（HEG, n = 10）。运动组大鼠进行8周的HIIT训练。随后进行行为测试和抽样指标测试。结果与正常安静组相比，运动组的体重和Lee指数明显下降，肥胖组的体重和Lee指数明显升高。Morris水迷宫实验表明，与CSG相比，HSG具有更长的潜伏期和更少的平台穿越次数。CEG潜伏期缩短，频率增加。与HSG相比，HEG的潜伏期更短，频率增加。组织染色显示HSG海马CA1区神经元数量减少、染色加深、排列混乱、尼氏体溶解，HIIT改善了这些病理改变。RT-qPCR结果显示，肥胖降低了海马组织中Sirt1基因的mRNA水平，而运动使其升高。Western blot分析显示，运动和肥胖分别调控SIRT1/PGC1α通路，运动上调其表达，肥胖下调其表达。结论8周HIIT可减轻肥胖大鼠海马神经元损伤和CI，其具体机制可能通过激活SIRT1/PGC1α通路改善神经元病理损伤，恢复认知功能。

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Effects of 8-Week High-Intensity Interval Training Intervention Regulating the SIRT1/PGC1α Pathway on Hippocampal Neuron Injury and Cognitive Impairment in Obese Rats

Background

Obesity can causes changes in cognitive function, leading to cognitive impairment (CI).

Objectives

This study aimed to explore the effects of high-intensity interval training (HIIT) on hippocampal neuronal damage, cognitive function, and the SIRT1/PGC1α pathway in obese rats and provide a theoretical basis for HIIT intervention in improving CI caused by obesity.

Methods

Rats with successful obesity modeling and rats of the same age were randomly divided into a normal quiet group (CSG, n = 10), regular exercise group (CEG, n = 10), high-fat quiet group (HSG, n = 10), and high-fat exercise group (HEG, n = 10). Rats in the exercise group underwent an 8-week (8-wk) HIIT training. Subsequently, behavioral testing and sampling indicator testing were conducted.

Results

Compared with the normal quiet group, the exercise group showed a significant decrease in body weight and Lee index, whereas the obesity group showed a significant increase. The Morris water maze experiment showed that compared with the CSG, the HSG had a longer latency period and a reduced number of platform crossings. The latency period of the CEG was shortened, and the frequency increased. Compared with the HSG, the HEG had a shorter latency period and an increase in frequency. Organizational staining showed that the HSG had reduced neuron number, deepened staining, chaotic arrangement, and Nissl body lysis in the hippocampal CA1 region, whereas HIIT improved these pathological changes. RT-qPCR showed obesity reduces the mRNA level of Sirt1 gene in hippocampal tissue, whereas exercise increases it. Western blot analysis showed exercise and obesity independently regulate the SIRT1/PGC1α pathway: exercise upregulates its expression, whereas obesity downregulates its expression.

Conclusions

An 8-wk HIIT can reduce hippocampal neuronal damage and CI in obese rats, and the specific mechanism may improve neuronal pathological damage and restore cognitive function by activating the SIRT1/PGC1α pathway.

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