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给予高胆固醇饮食的脑源性神经营养因子杂合子小鼠的感觉运动性能和大脑皮层神经化学效应。

Sensory‑motor performance and neurochemical effects in the cerebral cortex of brain‑derived neurotrophic factor heterozygous mice fed a high‑cholesterol diet.

机构信息

Department of Biophysics, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey.

Department of Biophysics, Faculty of Medicine, Aydın Adnan Menderes University, Aydın, Turkey.

出版信息

Acta Neurobiol Exp (Wars). 2023;83(1):1-9. doi: 10.55782/ane-2023-001.

DOI:10.55782/ane-2023-001
PMID:37078809
Abstract

Reports suggest that a high‑cholesterol diet may induce neuroinflammation, oxidative stress, and neurodegeneration in brain tissue. Brain‑derived neurotrophic factor (BDNF) might play a role in protecting against changes induced by high cholesterol. We aimed to assess behavioral correlates and biochemical alterations in the motor and sensory cortices following a high‑cholesterol diet under normal and reduced BDNF concentrations. C57Bl/6 strain, wild‑type (WT) and BDNF heterozygous (+/‑) mice were used to reveal the effects of endogenous BDNF concentrations. We compared diet and genotype effects using four experimental groups: WT and BDNF heterozygous (+/‑) groups of mice were each fed a normal or high‑cholesterol diet for 16 weeks. The cylinder test and wire hanging test were performed to evaluate neuromuscular deficits and cortical sensory‑motor functions, respectively. In addition, neuroinflammation was assessed by tumor necrosis factor alpha and interleukin 6 levels measured in the somatosensory and motor areas. Additionally, MDA levels and SOD and CAT activity were evaluated as oxidative stress parameters. Results showed that a high‑cholesterol diet significantly impaired behavioral performance in the BDNF (+/‑) group. Diet did not change the levels of neuroinflammatory markers in any of the groups. However, MDA levels, an indicator of lipid peroxidation, were significantly higher in the high‑cholesterol‑fed BDNF (+/‑) mice. The results suggest that BDNF levels might be a critical factor in determining the extent of neuronal damage induced in the neocortex by a high‑cholesterol diet.

摘要

报告表明,高胆固醇饮食可能会在脑组织中引起神经炎症、氧化应激和神经退行性变。脑源性神经营养因子(BDNF)可能在保护免受高胆固醇引起的变化方面发挥作用。我们旨在评估正常和 BDNF 浓度降低情况下,高胆固醇饮食后运动和感觉皮层的行为相关性和生化变化。使用 C57Bl/6 品系野生型(WT)和 BDNF 杂合子(+/ -)小鼠来揭示内源性 BDNF 浓度的影响。我们使用四个实验组比较饮食和基因型的影响:WT 和 BDNF 杂合子(+/ -)组的小鼠分别喂食正常或高胆固醇饮食 16 周。使用圆筒试验和悬线试验分别评估运动神经元和皮质感觉运动功能障碍。此外,通过测量躯体感觉和运动区域中的肿瘤坏死因子-α和白细胞介素 6 水平来评估神经炎症。此外,还评估 MDA 水平以及 SOD 和 CAT 活性作为氧化应激参数。结果表明,高胆固醇饮食显著损害了 BDNF(+/ -)组的行为表现。饮食在任何组中均未改变神经炎症标志物的水平。然而,高胆固醇喂养的 BDNF(+/ -)小鼠的 MDA 水平(脂质过氧化的指标)显着升高。结果表明,BDNF 水平可能是决定高胆固醇饮食引起新皮层神经元损伤程度的关键因素。

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