The Possible Neuroprotective Effect of Caffeic Acid on Cognitive Changes and Anxiety-Like Behavior Occurring in Young Rats Fed on High-Fat Diet and Exposed to Chronic Stress: Role of β-Catenin/GSK-3B Pathway

IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Molecular Neuroscience Pub Date : 2024-07-02 DOI:10.1007/s12031-024-02232-4
Norhan S. El-Sayed, Nehal Adel Khalil, Samar R. Saleh, Rania G. Aly, Marianne Basta
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Abstract

Lifestyle influences physical and cognitive development during the period of adolescence greatly. The most important of these lifestyle factors are diet and stress. Therefore, the aim of this study was to investigate the impact of high fat diet (HFD) and chronic mild stress on cognitive function and anxiety-like behaviors in young rats and to study the role of caffeic acid as a potential treatment for anxiety and cognitive dysfunction. Forty rats were assigned into 4 groups: control, HFD, HFD + stress, and caffeic acid-treated group. Rats were sacrificed after neurobehavioral testing. We detected memory impairment and anxiety-like behavior in rats which were more exaggerated in stressed rats. Alongside the behavioral changes, there were biochemical and histological changes. HFD and/or stress decreased hippocampal brain-derived neurotrophic factor (BDNF) levels and induced oxidative and inflammatory changes in the hippocampus. In addition, they suppressed Wnt/β-catenin pathway which was associated with activation of glycogen synthase kinase 3β (GSK3β). HFD and stress increased arginase 1 and inducible nitric oxide synthase (iNOS) levels as well. These disturbances were found to be aggravated in stressed rats than HFD group. However, caffeic acid was able to reverse these deteriorations leading to memory improvement and ameliorating anxiety-like behavior. So, the current study highlights an important neuroprotective role for caffeic acid that may guard against induction of cognitive dysfunction and anxiety disorders in adolescents who are exposed to HFD and/or stress.

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咖啡酸对高脂饮食并暴露于慢性应激的幼鼠认知变化和焦虑行为的可能神经保护作用:β-Catenin/GSK-3B通路的作用。
生活方式对青春期的身体和认知发展影响很大。其中最重要的生活方式因素是饮食和压力。因此,本研究旨在调查高脂饮食(HFD)和慢性轻度应激对幼鼠认知功能和焦虑样行为的影响,并研究咖啡酸作为治疗焦虑和认知功能障碍的潜在药物的作用。40 只大鼠被分为 4 组:对照组、高脂饮食组、高脂饮食 + 应激组和咖啡酸处理组。大鼠在神经行为测试后被处死。我们检测到大鼠的记忆损伤和焦虑样行为,这些行为在应激大鼠中更为显著。除行为变化外,还有生化和组织学变化。高脂饮食和/或应激降低了海马脑源性神经营养因子(BDNF)的水平,并诱发了海马的氧化和炎症变化。此外,它们还抑制了Wnt/β-catenin通路,而这与糖原合酶激酶3β(GSK3β)的激活有关。高脂饮食和应激也增加了精氨酸酶1和诱导型一氧化氮合酶(iNOS)的水平。与高饱和脂肪酸组相比,应激组大鼠的这些紊乱现象更为严重。然而,咖啡酸能够逆转这些恶化,从而改善记忆,并改善焦虑样行为。因此,目前的研究强调了咖啡酸对神经的重要保护作用,它可以防止青少年在高纤维食物摄入和/或压力下诱发认知功能障碍和焦虑症。
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来源期刊
Journal of Molecular Neuroscience
Journal of Molecular Neuroscience 医学-神经科学
CiteScore
6.60
自引率
3.20%
发文量
142
审稿时长
1 months
期刊介绍: The Journal of Molecular Neuroscience is committed to the rapid publication of original findings that increase our understanding of the molecular structure, function, and development of the nervous system. The criteria for acceptance of manuscripts will be scientific excellence, originality, and relevance to the field of molecular neuroscience. Manuscripts with clinical relevance are especially encouraged since the journal seeks to provide a means for accelerating the progression of basic research findings toward clinical utilization. All experiments described in the Journal of Molecular Neuroscience that involve the use of animal or human subjects must have been approved by the appropriate institutional review committee and conform to accepted ethical standards.
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