有氧运动通过调节DAPK1/CDKN2A/REDD1/FoXO1/FasL信号通路减轻D-半乳糖诱导衰老小鼠海马神经元凋亡,The FASEB Journal

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有氧运动通过调节DAPK1/CDKN2A/REDD1/FoXO1/FasL信号通路减轻D-半乳糖诱导衰老小鼠海马神经元凋亡
The FASEB Journal ( IF 4.4 ) Pub Date : 2023-09-28 , DOI: 10.1096/fj.202300847rr
Yang Liu ₁ , Wen Guo ₁ , Si-Lu Hong ₁

Affiliation

大脑衰老是神经退行性疾病最重要的危险因素，细胞凋亡异常与神经元功能障碍有关。具体来说，研究发现运动可以有效抑制海马神经元凋亡，但其分子机制尚不清楚。在本研究中，我们基于DAPK1可能与神经退行性疾病中神经元死亡相关的最新数据，研究了有氧运动对衰老小鼠海马神经元凋亡的影响以及DAPK1及其下游通路的潜在参与。衰老小鼠接受8周的有氧训练。行为测试后，对海马样本进行组织学和生化检查，以检测病理变化、神经元凋亡以及 mRNA 和蛋白质水平。我们发现运动干预改善了空间记忆并减轻了大脑中的神经元凋亡。值得注意的是，运动下调 DAPK1 表达并抑制 Fas 死亡受体反式激活和海马体线粒体凋亡途径。这些结果为定期运动通过调节 DAPK1 通路对抗大脑衰老的保护作用提供了新的线索。

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Aerobic exercise mitigates hippocampal neuronal apoptosis by regulating DAPK1/CDKN2A/REDD1/FoXO1/FasL signaling pathway in D-galactose-induced aging mice

Brain aging is the most important risk factor for neurodegenerative disorders, and abnormal apoptosis is linked to neuronal dysfunction. Specifically, studies have found that exercise effectively inhibits hippocampal neuronal apoptosis, while the molecular mechanism remains unclear. In the present study, we investigated the impact of aerobic exercise on hippocampal neuronal apoptosis in aging mice and the potential involvement of DAPK1 and its downstream pathways based on recent data that DAPK1 may be associated with neuronal death in neurodegenerative diseases. Senescent mice were subjected to 8 weeks of Aerobic training. Following behavioral testing, hippocampal samples were examined histologically and biochemically to detect pathological changes, neuronal apoptosis, and mRNA and protein levels. We found that the exercise intervention improved spatial memory and alleviated neuronal apoptosis in the brain. Notably, exercise down-regulated DAPK1 expression and inhibited Fas death receptor transactivation and the mitochondrial apoptotic pathway in the hippocampus. These results shed new light on the protective effect of regular exercise against brain aging though modulating the DAPK1 pathway.

更新日期：2023-09-28

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