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.
摘要：
生活方式极大地影响了青春期的身体和认知发展。这些生活方式因素中最重要的是饮食和压力。因此,本研究的目的是研究高脂饮食(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.将40只大鼠分为4组：对照组，HFD,HFD+应力,和咖啡酸治疗组。在神经行为测试后处死大鼠。我们在大鼠中检测到记忆障碍和焦虑样行为，而在应激大鼠中更为夸张。除了行为变化，有生化和组织学变化。HFD和/或应激降低海马脑源性神经营养因子（BDNF）水平，并诱导海马的氧化和炎症变化。此外,它们抑制了与糖原合成酶激酶3β（GSK3β）激活相关的Wnt/β-catenin通路。HFD和胁迫也增加了精氨酸酶1和诱导型一氧化氮合酶（iNOS）的水平。发现这些干扰在应激大鼠中比HFD组加重。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。所以,本研究强调了咖啡酸的重要神经保护作用,在暴露于HFD和/或应激的青少年中,咖啡酸可以预防认知功能障碍和焦虑障碍的诱导.
