疲劳大鼠模型的认知障碍和前额叶TGF-β1升高
Cognitive impairment and prefrontal TGF-β1 elevation in a rat model of fatigue.
摘要(中文译文)
慢性疲劳综合征（CFS）是一种病因不明的复杂疾病，以休息后不能缓解的持续性疲劳为特征，并伴有认知功能障碍。尽管细胞因子失调被认为参与CFS的发病机制，但抗炎性转化生长因子β1（TGF-β1）的作用仍不明确。本研究在为期10天反复睡眠剥夺并间歇休息诱导的疲劳大鼠模型中，探讨了中枢和外周TGF-β1失调与认知功能的关系。大鼠被随机分为对照组和疲劳组。在疲劳负荷程序结束后进行行为学测试，包括旷场实验和Y迷宫实验。检测外周和中枢TGF-β1水平。疲劳组大鼠白天短期运动活性未见改变，但在旷场实验中焦虑样行为显著增加。在Y迷宫实验中，疲劳组与对照组相比自发交替率明显降低。此外，疲劳大鼠前额叶皮质TGF-β1水平升高，而外周和纹状体TGF-β1在两组间均无差异。这些发现表明，为期10天反复睡眠剥夺并间歇休息的疲劳模型可诱导认知损害和焦虑样行为增加，并伴有选择性前额叶TGF-β1上调。前额叶TGF-β1升高与认知缺陷同时出现，提示中枢TGF-β1信号可能在精神疲劳的病理生理学中发挥作用，尽管这种关系的确切性质仍有待阐明。
Abstract
Chronic fatigue syndrome (CFS) is a complex disorder of unknown etiology, characterized by persistent fatigue unrelieved by rest and accompanied by cognitive dysfunction. While dysregulated cytokines are implicated in CFS pathogenesis, the role of anti-inflammatory transforming growth factor β1 (TGF-β1) remains poorly defined. This study investigated central and peripheral TGF-β1 dysregulation and cognitive function in a rat model of fatigue induced by 10-day repetitive sleep deprivation with intermittent rest. Rats were randomly divided into the control group and the fatigue group. Behavioral tests including open field test and Y-maze test were performed after the end of fatigue-loading procedure. Peripheral and central TGF-β1 levels were detected. Rats in the fatigue group exhibited unchanged daytime short-term locomotor activity but significantly increased anxiety-like behavior in the open field test. In the Y-maze test, the fatigue group showed markedly reduced spontaneous alternation rates compared to controls. Furthermore, prefrontal cortical TGF-β1 levels were elevated in fatigued rats, whereas neither peripheral nor striatal TGF-β1 differed between groups. These findings demonstrate that the 10-day repetitive sleep deprivation with intermittent rest fatigue model induces cognitive impairment and increased anxiety-like behavior, with selective prefrontal TGF-β1 upregulation. The concomitant elevation of prefrontal TGF-β1 and cognitive deficits suggests a potential role for central TGF-β1 signaling in the pathophysiology of mental fatigue, although the precise nature of this relationship remains to be elucidated.
如何引用
AMA
Yingru Wu, Xuan Wen, Zeman Fang, Jinling Zhang, Handi Zhang. Cognitive impairment and prefrontal TGF-β1 elevation in a rat model of fatigue.. Frontiers in psychiatry. 2026; doi:10.3389/fpsyt.2026.1841951.
APA
Yingru Wu, Xuan Wen, Zeman Fang, Jinling Zhang, Handi Zhang (2026). Cognitive impairment and prefrontal TGF-β1 elevation in a rat model of fatigue.. Frontiers in psychiatry. https://doi.org/10.3389/fpsyt.2026.1841951
GB/T 7714
Yingru Wu, Xuan Wen, Zeman Fang, Jinling Zhang, Handi Zhang. Cognitive impairment and prefrontal TGF-β1 elevation in a rat model of fatigue.[J]. Frontiers in psychiatry, 2026 doi:10.3389/fpsyt.2026.1841951.
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