亨廷顿舞蹈症（HD）是一种极其有害的常染色体遗传性神经退行性疾病。运动功能障碍、精神障碍和认知缺陷是该病的特征。当前的研究检查了 6-姜烯酚是否对 3-硝基丙酸 (3-NPA) 诱导的大鼠 HD 具有保护作用。总共 30 只雄性 Wistar 大鼠接受了 6-姜烯酚（每次口服 10 和 20 毫克/千克）注射 3-NPA（10 mg/kg i.p.）前一小时，持续 15 天。进行了行为测试，包括窄梁行走、旋转杆测试和握力测试。评估了促进氧化应激的生化测试[超氧化物歧化酶（SOD）、还原型谷胱甘肽（GSH）、过氧化氢酶（CAT）和丙二醛（MDA）]，包括神经递质血清素（5-HT）、多巴胺（DA）、去甲肾上腺素（NE）的变化)、高香草酸 (HVA)、(3,4-二羟基苯乙酸 (DOPAC)、γ-氨基丁酸 (GABA) 和 5-羟基吲哚乙酸 (5-HIAA)、核因子 kappa-B (NF-κB) 、肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β)、IL-6、脑源性神经营养因子 (BDNF) 和核因子红细胞 2 相关因子 2 (Nrf2)。使用 AutoDock 工具将 shogaol 对接至 TNF-α (2AZ5)、NF-κB (1SVC)、BDNF) [1B8M] 和 Nrf2 [5FZN] 蛋白的活性位点。与 3 组相比，6-shogaol 组显着改善了行为活动-注射NPA的对照大鼠。此外，3-NPA 诱导的神经递质、生化和神经炎症指数显着改变，而 6-shogaol 可以有效逆转这种变化。 6-姜烯酚在 -9.271 (BDNF) kcal/mol 处表现出有利的负结合能。本研究证明了 6-姜烯酚在实验动物范例中对 3-NPA 诱导的大鼠 HD 的神经保护作用。尽管还需要更多的研究来明确证实，但所提出的机制得到了免疫组织化学分析和蛋白质印迹的支持。版权所有：© 2024 Jambi 等人。这是一篇根据知识共享署名许可条款分发的开放获取文章，允许在任何媒体上不受限制地使用、分发和复制，前提是注明原始作者和来源。

Huntington's disease (HD) is an extremely harmful autosomal inherited neurodegenerative disease. Motor dysfunction, mental disorder, and cognitive deficits are the characteristic features of this disease. The current study examined whether 6-shogaol has a protective effect against 3-Nitropropionic Acid (3-NPA)-induced HD in rats.A total of thirty male Wistar rats received 6-shogaol (10 and 20 mg/kg, per oral) an hour before injection of 3-NPA (10 mg/kg i.p.) for 15 days. Behavioral tests were performed, including narrow beam walk, rotarod test, and grip strength test. Biochemical tests promoting oxidative stress were evaluated [superoxide dismutase (SOD), reduced glutathione (GSH), catalase (CAT) and malondialdehyde (MDA)], including changes to neurotransmitters serotonin (5-HT), dopamine (DA), norepinephrine (NE), homovanillic acid (HVA), (3,4-dihydroxyphenylacetic acid (DOPAC), γ-aminobutyric acid (GABA), and 5-hydroxy indole acetic acid (5-HIAA), nuclear factor kappa-B (NF-κB), tumor necrosis factor-α (TNF-α), interleukins-1β (IL-1β), IL-6, brain-derived neurotrophic factor (BDNF), and nuclear factor erythroid 2-related factor 2 (Nrf2). The 6-shogaol was docked to the active site of TNF-α (2AZ5), NF-κB (1SVC), BDNF) [1B8M], and Nrf2 [5FZN] proteins using AutoDock tools.The 6-shogaol group significantly improved behavioral activity over the 3-NPA-injected control rats. Moreover, 3-NPA-induced significantly altered neurotransmitters, biochemical and neuroinflammatory indices, which could efficiently be reversed by 6-shogaol. The 6-shogaol showed favorable negative binding energies at -9.271 (BDNF) kcal/mol.The present investigation demonstrated the neuroprotective effects of 6-shogaol in an experimental animal paradigm against 3-NPA-induced HD in rats. The suggested mechanism is supported by immunohistochemical analysis and western blots, although more research is necessary for definite confirmation.Copyright: © 2024 Jambi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.