Obesity, which has become one of the main health problems, results from irregular and unhealthy nutrition. In particular, an increase in the intake of high-fat foods leads to obesity and associated disorders. It is noteworthy to specify that obese individuals have memory problems. This study aims to examine the effects of high-fat diet on hippocampus, with stereological, histopathological methods and STRING bioinformatic tool. Female Adult Sprague Dawley rats (n = 20) were equally divided into control (CONT) and high-fat diet (HFD) groups. The control group was given standard rat pellet feed, while the high-fat diet group was fed with a 40 % fat content for 2 months. Following the feeding program, rats were sacrificed. The collected blood samples were analyzed biochemically to determine the level of oxidative stress while performing a stereological and histopathological examination of the brain tissues. Functional protein-protein networks for BDNF, C-Fos, CAT, LPO, SOD and MPO by gene ontology (GO) enrichment analysis were evaluated. The number of neurons decreased in the HFD group compared to the CONT group. Damage to the histological structure of the hippocampus region; such as degenerate neurons, damaged mitochondria and extended cisterns of the endoplasmic reticulum was observed. Although C-Fos level and oxidative stress parameters increased in HFD group, BDNF level decreased. While BDNF and C-Fos were observed in pathways related to neuron death, oxidative stress and memory, BDNF was pronounced in the mitochondria, and C-Fos in the endoplasmic reticulum. This study shows that changes in both BDNF and C-Fos levels in obesity due to high-fat diet increase oxidative stress and cause neuron damage in the hippocampus.

中文翻译：

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高脂饮食诱导的肥胖大鼠海马神经细胞损失——探索蛋白质网络、超微结构、生化和生物信息标记


肥胖已成为主要的健康问题之一，其根源在于营养不规律和不健康。特别是，高脂肪食物摄入量的增加会导致肥胖和相关疾病。值得注意的是，肥胖者存在记忆问题。本研究旨在通过体视学、组织病理学方法和STRING生物信息学工具探讨高脂肪饮食对海马体的影响。雌性成年斯普拉道利大鼠（n = 20）被平均分为对照组（CONT）和高脂饮食（HFD）组。对照组给予标准大鼠颗粒饲料，高脂饲料组给予40%脂肪含量喂养2个月。按照喂养程序，处死大鼠。对收集的血液样本进行生化分析，以确定氧化应激水平，同时对脑组织进行体视学和组织病理学检查。通过基因本体（GO）富集分析评估了 BDNF、C-Fos、CAT、LPO、SOD 和 MPO 的功能蛋白-蛋白网络。与 CONT 组相比，HFD 组的神经元数量减少。海马区组织学结构受损；观察到神经元退化、线粒体受损和内质网池扩大等。 HFD组虽然C-Fos水平和氧化应激参数升高，但BDNF水平降低。虽然在与神经元死亡、氧化应激和记忆相关的通路中观察到 BDNF 和 C-Fos，但 BDNF 明显存在于线粒体中，C-Fos 在内质网中明显。这项研究表明，高脂肪饮食导致的肥胖症中 BDNF 和 C-Fos 水平的变化会增加氧化应激并导致海马神经元损伤。