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百里醌通过调节氧化应激、炎症和细胞凋亡，控制了食用高脂饮食大鼠的肥胖，并增强了其认知和记忆能力。

Thymoquinone controlled obesity and invigorated cognitive and memory performance in rats consuming a high-fat diet via modulating oxidative stress, inflammation and apoptosis.

作者信息

Mostafa Mostafa D, Amer Maggie E, ElKomy Magda A, Othman Azza I, El-Missiry Mohamed A

机构信息

Department of Zoology, Faculty of Science, Mansoura University, Mansoura, Egypt.

出版信息

Sci Rep. 2025 Jun 20;15(1):20171. doi: 10.1038/s41598-025-05716-4.

DOI:10.1038/s41598-025-05716-4
PMID:40542063
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12181254/
Abstract

The current study investigated the mitigating effects of thymoquinone (TQ) against high-fat diet (HFD)-mediated brain injury, cognitive and memory impairment, and the underlying mechanisms. Twenty-four adult male Wistar rats were divided into four groups of six rats each. Rats were fed HFD for 12 weeks to induce obesity. On the 9th week, TQ was administered orally to obese rats for four weeks. The effects of TQ were estimated by neurobehavioral testing, biochemical analysis, DNA damage, molecular docking, and histopathological examination of brains and visceral fat. TQ reduced body weight, body weight gain and adipocyte size, improved hyperlipidemia, and normalized the levels of leptin and adiponectin. TQ significantly attenuated the increase in HbA1c percent and insulin resistance. TQ decreased the accumulation of amyloid-β and tau proteins and improved the levels of neurotransmitters in the brains of obese rats. TQ-treated obese rats showed improved thickening of the pyramidal cell layer in the hippocampus and improved cognitive function and memory impairments. Molecular docking analysis indicated that TQ exhibited a marked affinity for inhibiting binding sites of tau and amyloid-β proteins. Furthermore, TQ controlled oxidative stress and enhanced the Nrf2 expression in the pyramidal cell layer and the activity of HO-1, SOD, and CAT in the brain. The restoration of redox balance by TQ was associated with normalization of inflammatory indicators and alleviation of DNA damage in the brains of HFD-treated animals. These changes contributed to the normalization of mitochondrial apoptotic pathway mediators (p53, Bcl-2, Bax, and caspase-3) and maintained the histological structure of the hippocampus. In conclusion, TQ attenuated brain injury, cognitive impairment, and memory deficit with improvement of body weight gain and metabolic status in obese rats through interrelated biological processes, including regulation of redox balance, inflammatory response, neurotransmitter equilibrium, and regression of DNA injury and apoptosis.

摘要

本研究调查了百里醌（TQ）对高脂饮食（HFD）介导的脑损伤、认知和记忆障碍的缓解作用及其潜在机制。将24只成年雄性Wistar大鼠分为四组，每组6只。给大鼠喂食HFD 12周以诱导肥胖。在第9周，对肥胖大鼠口服TQ，持续四周。通过神经行为测试、生化分析、DNA损伤、分子对接以及对大脑和内脏脂肪的组织病理学检查来评估TQ的作用。TQ降低了体重、体重增加和脂肪细胞大小，改善了高脂血症，并使瘦素和脂联素水平恢复正常。TQ显著减轻了糖化血红蛋白百分比的升高和胰岛素抵抗。TQ减少了肥胖大鼠大脑中淀粉样β蛋白和tau蛋白的积累，并改善了神经递质水平。经TQ处理的肥胖大鼠海马锥体细胞层增厚得到改善，认知功能和记忆障碍也得到改善。分子对接分析表明，TQ对抑制tau蛋白和淀粉样β蛋白的结合位点具有显著亲和力。此外，TQ控制了氧化应激，增强了锥体细胞层中Nrf2的表达以及大脑中HO-1、SOD和CAT的活性。TQ恢复氧化还原平衡与HFD处理动物大脑中炎症指标的正常化以及DNA损伤的减轻有关。这些变化有助于线粒体凋亡途径介质（p53、Bcl-2、Bax和caspase-3）的正常化，并维持海马的组织结构。总之，TQ通过相互关联的生物学过程，包括调节氧化还原平衡、炎症反应、神经递质平衡以及DNA损伤和凋亡的消退，减轻了肥胖大鼠的脑损伤、认知障碍和记忆缺陷，并改善了体重增加和代谢状态。

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本文引用的文献

[1]
Thymoquinone ameliorate oxidative stress, GABAergic neuronal depletion and memory impairment through Nrf2/ARE signaling pathway in the dentate gyrus following cypermethrin administration.

BMC Neurosci. 2024-9-27

[2]
Melatonin rescues pregnant female mice and their juvenile offspring from high fat diet-induced alzheimer disease neuropathy.

Heliyon. 2024-8-24

[3]
Glutamate-Mediated Excitotoxicity in the Pathogenesis and Treatment of Neurodevelopmental and Adult Mental Disorders.

Int J Mol Sci. 2024-6-13

[4]
Thymoquinone attenuates diabetes-induced hepatic damage in rat via regulation of oxidative/nitrosative stress, apoptosis, and inflammatory cascade with molecular docking approach.

Sci Rep. 2024-6-6

[5]
Probucol mitigates high-fat diet-induced cognitive and social impairments by regulating brain redox and insulin resistance.

Front Neurosci. 2024-4-23

[6]
Interaction of high-fat diet and brain trauma alters adipose tissue macrophages and brain microglia associated with exacerbated cognitive dysfunction.

J Neuroinflammation. 2024-4-29

[7]
Neuroprotective effect of Withania somnifera leaves extract nanoemulsion against penconazole-induced neurotoxicity in albino rats via modulating TGF-β1/Smad2 signaling pathway.

Inflammopharmacology. 2024-6

[8]
Phytomedicine for neurodegenerative diseases: The road ahead.

Phytother Res. 2024-6

[9]
Impact of high-fat diet on cognitive behavior and central and systemic inflammation with aging and sex differences in mice.

Brain Behav Immun. 2024-5

[10]
The obesity-autophagy-cancer axis: Mechanistic insights and therapeutic perspectives.

Semin Cancer Biol. 2024-2

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