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代谢综合征加剧了海马内注射淀粉样β 1-42 导致的大鼠识别记忆损伤和氧化应激反应。

Metabolic Syndrome Exacerbates the Recognition Memory Impairment and Oxidative-Inflammatory Response in Rats with an Intrahippocampal Injection of Amyloid Beta 1-42.

机构信息

Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, Puebla, PUE, Mexico.

Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.

出版信息

Oxid Med Cell Longev. 2018 Aug 1;2018:1358057. doi: 10.1155/2018/1358057. eCollection 2018.

DOI:10.1155/2018/1358057
PMID:30154946
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6092993/
Abstract

An important worldwide health problem as the result of current lifestyle is metabolic syndrome (MS). It has been shown that MS induced by a high-calorie diet (HCD) in rats produces cognitive deterioration in the novel object recognition test (NORt) and decreases synaptic connections and dendritic order in the hippocampus and temporal cortex. However, it is unknown whether MS induced by an HCD participates in the cognitive process observed with the injection of A into the hippocampus of rats as a model of Alzheimer disease (AD). The induction of MS in rats produces a deterioration in NORt; however, rats with MS injected with A show a major deterioration in the cognitive process. This event could be explained by the increment in the oxidative stress in both cases studied (MS and A): together, the hippocampus and temporal cortex produce an enhancer effect. In the same way, we observed an increment in interleukin-1, TNF-, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and A. We can conclude that MS might play a key role in the apparition and development of cognitive disorders, including AD. We propose that metabolic theory is important to explain the apparition of cognitive diseases.

摘要

作为当前生活方式导致的一个重要的全球健康问题,代谢综合征(MS)受到了广泛关注。研究表明,高热量饮食(HCD)诱导的 MS 可导致大鼠在新物体识别测试(NORt)中认知能力下降,并减少海马体和颞叶皮质中的突触连接和树突排列。然而,目前尚不清楚 HCD 诱导的 MS 是否会参与到向大鼠海马体注射 A 作为阿尔茨海默病(AD)模型所观察到的认知过程中。MS 诱导会导致 NORt 认知能力下降;然而,注射 A 后 MS 大鼠的认知过程会出现严重恶化。这种情况可以通过两种情况下氧化应激的增加来解释(MS 和 A):海马体和颞叶皮质一起产生增强效应。同样,我们观察到白细胞介素-1、TNF-和 GFAP 的增加,表明 MS 和 A 的组合加剧了炎症反应。我们可以得出结论,MS 可能在认知障碍(包括 AD)的出现和发展中起关键作用。我们提出代谢理论对于解释认知疾病的出现很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/86f0/6092993/bc9de42af3af/OMCL2018-1358057.007.jpg
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