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大黄素对阿尔茨海默病痴呆的神经保护、抗炎和抗纤维化作用:一项系统评价

Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer's Dementia: A Systematic Review.

作者信息

Saha Priyanka, Ahmad Faraz

机构信息

Department of Biotechnology, School of Bio Sciences and Technology (SBST), Vellore Institute of Technology, Vellore 632014, India.

出版信息

ACS Omega. 2024 Feb 7;9(7):7296-7309. doi: 10.1021/acsomega.3c07178. eCollection 2024 Feb 20.

DOI:10.1021/acsomega.3c07178
PMID:38405501
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10882671/
Abstract

: Alzheimer's disease (AD) is among the major causes of dementia in the elderly and exerts tremendous clinical, psychological and socio-economic constraints. Currently, there are no effective disease-modifying/retarding anti-AD agents. Emodin is a bioactive phytochemical with potent multimodal anti-inflammatory, antioxidant, and antifibrillogenic properties. In particular, emodin may result in significant repression of the pathogenic mechanisms underlying AD. The purpose of this review is to accumulate and summarize all the primary research data evaluating the therapeutic actions of emodin in AD pathogenesis. : The search, selection, and retrieval of pertinent primary research articles were systematically performed using a methodically designed approach. A variety of keyword combinations were employed on online scholarly web-databases. Strict preset inclusion and exclusion criteria were used to select the retrieved studies. Data from the individual studies were summarized and compiled into different sections, based upon their findings. : Cellular and animal research indicates that emodin exerts robust multimodal neuroprotection in AD. While emodin effectively prevents tau and amyloid-beta (Aβ) oligomerization, it also mitigates their neurotoxicity by attenuating neuroinflammatory, oxidative, and bioenergetic defects. Evidences for emodin-mediated enhancements in memory, learning, and cognition were also found in the literature. : Emodin is a potential anti-AD dietary supplement; however, further studies are warrantied to thoroughly understand its target players and mechanisms. Moreover, human clinical data on emodin-mediated amelioration of AD phenotype is largely lacking, and must be addressed in the future. Lastly, the safety of exogenously supplemented emodin must be thoroughly evaluated.

摘要

阿尔茨海默病(AD)是老年人痴呆的主要病因之一,带来了巨大的临床、心理和社会经济负担。目前,尚无有效的疾病修饰/延缓抗AD药物。大黄素是一种具有多种生物活性的植物化学物质,具有强大的多模式抗炎、抗氧化和抗纤维原性特性。特别是,大黄素可能会显著抑制AD的致病机制。本综述的目的是积累和总结所有评估大黄素在AD发病机制中治疗作用的主要研究数据。:采用精心设计的方法系统地进行相关主要研究文章的检索、筛选和获取。在在线学术网络数据库上使用了各种关键词组合。使用严格预设的纳入和排除标准来选择检索到的研究。根据各项研究的结果,将其数据进行总结并汇编到不同的部分。:细胞和动物研究表明,大黄素在AD中发挥强大的多模式神经保护作用。大黄素不仅能有效防止tau蛋白和β淀粉样蛋白(Aβ)寡聚化,还能通过减轻神经炎症、氧化和生物能量缺陷来减轻它们的神经毒性。文献中也发现了大黄素介导的记忆、学习和认知增强的证据。:大黄素是一种潜在的抗AD膳食补充剂;然而,需要进一步研究以全面了解其作用靶点和机制。此外,关于大黄素介导改善AD表型的人体临床数据在很大程度上缺乏,未来必须加以解决。最后,必须全面评估外源性补充大黄素的安全性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ea/10882671/0ce2104bfc24/ao3c07178_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ea/10882671/cf3c5cd5f7e3/ao3c07178_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ea/10882671/ce2d43b0ecd6/ao3c07178_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ea/10882671/0ce2104bfc24/ao3c07178_0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ea/10882671/cf3c5cd5f7e3/ao3c07178_0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ea/10882671/ce2d43b0ecd6/ao3c07178_0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1ea/10882671/0ce2104bfc24/ao3c07178_0003.jpg

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