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口香糖通过影响脑源性神经营养因子(BDNF)和核因子κB(NF-κB)对氯化铝诱导的大鼠阿尔茨海默病模型的保护作用

The Protective Effects of Gum in a Rat Model of Aluminum Chloride-Induced Alzheimer's Disease via Affecting BDNF and NF-kB.

作者信息

Gravandi Mohammad Mehdi, Hosseini Seyede Zahra, Alavi Seyede Darya, Noori Tayebeh, Sureda Antoni, Amirian Roshanak, Farzaei Mohammad Hosein, Shirooie Samira

机构信息

Student Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Pharmaceutical Sciences Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.

出版信息

Iran J Pharm Res. 2024 Jun 22;23(1):e142203. doi: 10.5812/ijpr-142203. eCollection 2024 Jan-Dec.

DOI:10.5812/ijpr-142203
PMID:39005733
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11246649/
Abstract

Alzheimer's disease (AD) is a neurodegenerative condition characterized by progressive cognitive deterioration, including deficits in memory and other cognitive functions. Oxidative stress and free radical damage play significant roles in its pathogenesis. This study aimed to investigate the potential anti-inflammatory and neuroprotective effects of gum (administered at doses of 50 and 100 mg/kg for 14 days) in a rat model of AD induced by aluminum chloride (AlCl). Behavioral changes were assessed using open field, passive avoidance, and elevated plus maze tests. Additionally, nitrite levels, nuclear factor-kappa B (NF-κB), brain-derived neurotrophic factor (BDNF), and immunostaining were evaluated. Administration of gum significantly increased step-through latency in the passive avoidance test (P < 0.01 and P < 0.001), enhanced mobility in the open field test (P < 0.01 and P < 0.001), and reduced anxiety-like behaviors in the elevated plus maze (P < 0.001) compared to the AlCl group. Treatment with the gum partially normalized the elevated levels of NF-κB and the decreased levels of BDNF caused by AlCl exposure. Our findings suggest that gum administration may alleviate oxidative stress, neuroinflammation, and cognitive impairment in AD rats.

摘要

阿尔茨海默病(AD)是一种神经退行性疾病,其特征为进行性认知功能衰退,包括记忆和其他认知功能缺陷。氧化应激和自由基损伤在其发病机制中起重要作用。本研究旨在探讨[某种胶](以50和100毫克/千克的剂量给药14天)在氯化铝(AlCl)诱导的AD大鼠模型中的潜在抗炎和神经保护作用。使用旷场试验、被动回避试验和高架十字迷宫试验评估行为变化。此外,还评估了亚硝酸盐水平、核因子-κB(NF-κB)、脑源性神经营养因子(BDNF)和免疫染色。与AlCl组相比,给予[某种胶]显著增加了被动回避试验中的穿通潜伏期(P < 0.01和P < 0.001),增强了旷场试验中的活动能力(P < 0.01和P < 0.001),并减少了高架十字迷宫中的焦虑样行为(P < 0.001)。用[某种胶]治疗部分使由AlCl暴露引起的NF-κB水平升高和BDNF水平降低恢复正常。我们的研究结果表明,给予[某种胶]可能减轻AD大鼠的氧化应激、神经炎症和认知障碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/0be8874df3b2/ijpr-23-1-142203-i005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/cdad3d48d420/ijpr-23-1-142203-i001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/408fd9210f74/ijpr-23-1-142203-i002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/316a52fb6c0b/ijpr-23-1-142203-i003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/5c26acb5608a/ijpr-23-1-142203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/d2c7e815aa5c/ijpr-23-1-142203-i004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/0be8874df3b2/ijpr-23-1-142203-i005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/cdad3d48d420/ijpr-23-1-142203-i001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/408fd9210f74/ijpr-23-1-142203-i002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/316a52fb6c0b/ijpr-23-1-142203-i003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/5c26acb5608a/ijpr-23-1-142203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/d2c7e815aa5c/ijpr-23-1-142203-i004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef92/11246649/0be8874df3b2/ijpr-23-1-142203-i005.jpg

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本文引用的文献

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Neuroprotective Effects of Phytochemicals against Aluminum Chloride-Induced Alzheimer's Disease through ApoE4/LRP1, Wnt3/β-Catenin/GSK3β, and TLR4/NLRP3 Pathways with Physical and Mental Activities in a Rat Model.植物化学物质通过载脂蛋白E4/低密度脂蛋白受体相关蛋白1、Wnt3/β-连环蛋白/糖原合成酶激酶3β和Toll样受体4/NLRP3信号通路对氯化铝诱导的大鼠阿尔茨海默病模型产生神经保护作用并伴有身心活动。
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The Pivotal Role of NF-kB in the Pathogenesis and Therapeutics of Alzheimer's Disease.NF-κB 在阿尔茨海默病发病机制和治疗中的关键作用。
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