Targeting Nrf2 signaling pathway by quercetin in the prevention and treatment of neurological disorders: An overview and update on new developments

神经保护 神经炎症 医学 冲程(发动机) 创伤性脑损伤 氧化应激 神经科学 药理学 生物信息学 疾病 生物 精神科 内科学 机械工程 工程类
作者
Mohammad Yasin Zamanian,Afsaneh Soltani,Zahra Khodarahmi,Ameer A. Alameri,Athemar M. R. Alwan,Andrés Alexis Ramírez‐Coronel,Rasha Fadhel Obaid,Munther Abosaooda,Mahsa Heidari,Maryam Golmohammadi,Mahdieh Anoush
出处
期刊:Fundamental & Clinical Pharmacology [Wiley]
卷期号:37 (6): 1050-1064 被引量:29
标识
DOI:10.1111/fcp.12926
摘要

Abstract Background: Neurological disorders (NLDs) are widely acknowledged as a significant public health concern worldwide. Stroke, Alzheimer's disease (AD), and traumatic brain injury (TBI) are three of these disorders that have sparked major study attention. Neurological dysfunction, protein buildup, oxidation and neuronal injury, and aberrant mitochondria are all prevalent neuropathological hallmarks of these disorders. The signaling cascade of nuclear factor erythroid 2 related factor 2 (Nrf2) shares all of them as a common target. Several studies have found that overexpression of Nrf2 is a promising treatment method in NLDs. Effective treatment of these disorders continues to be a universal concern regardless of various medicines. In order to treat a variety of neurological problems, organic remedies may provide an alternative treatment. It has been demonstrated that polyphenols like quercetin (Que) offer considerable capabilities for treating NLDs. One of Que's greatest key targets, Nrf2, has the capacity to control the production of a number of cytoprotective enzymes that exhibit neuroprotective, detoxifying, and antioxidative effects. Additionally, Que enhanced the expression of Nrf2 and inhibited alterations in the shape and death of neurons in the hippocampus. Objective: In this review, we have focused on Que's medicinal prospects as a neuroprotective drug. Methods: PubMed, Scopus, Science Direct, and Google Scholar were used to search articles for this study. Results: The findings of this research demonstrate that (1) Que protected the blood‐brain barrier via stimulating Nrf2 in animal stroke, which alleviated ischemic reperfusion and motor dysfunction. (2) By triggering the Nrf2 pathway, Que reduced the neuroinflammation and oxidative damage brought on by TBI in the cortex. (3) In an experimental model of AD, Que enhanced cognitive function by decreasing A1‐4, antioxidant activity, and Nrf2 levels in the brain. Conclusion: We discuss recent research on Que‐mediated Nrf2 expression in the management of several NLDs in this paper.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
1秒前
后知后觉完成签到 ,获得积分10
1秒前
24K纯路人完成签到 ,获得积分10
1秒前
万能图书馆应助暴富小羊采纳,获得10
1秒前
科研通AI6.2应助Doctor_Peng采纳,获得10
2秒前
2秒前
3秒前
3秒前
4秒前
白榆发布了新的文献求助10
4秒前
卢不羁发布了新的文献求助10
4秒前
隐形冬寒发布了新的文献求助10
4秒前
4秒前
11发布了新的文献求助10
4秒前
Findway发布了新的文献求助10
4秒前
ding应助勇往直前采纳,获得10
5秒前
GJJJJJJJ发布了新的文献求助10
5秒前
二艺发布了新的文献求助10
5秒前
huang应助优雅的狂妄采纳,获得10
6秒前
Ava应助质子耦合电子迁移采纳,获得10
6秒前
6秒前
nihao完成签到,获得积分10
6秒前
6秒前
由心向也发布了新的文献求助10
7秒前
7秒前
7秒前
馨馨的科科应助幸福遥采纳,获得10
7秒前
向月亮出发rq完成签到,获得积分10
8秒前
xiaochong完成签到,获得积分10
9秒前
sayso发布了新的文献求助10
9秒前
六六完成签到 ,获得积分10
9秒前
GZU_Bluest_LJS完成签到 ,获得积分10
9秒前
木头完成签到,获得积分10
9秒前
太阳发布了新的文献求助30
9秒前
研dog完成签到,获得积分10
10秒前
在水一方应助太阳娃娃采纳,获得10
10秒前
10秒前
星1完成签到 ,获得积分10
11秒前
11秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Principles of town planning: translating concepts to applications 1000
内視鏡的に摘除しえた十二指腸乳頭部腫瘍の2例 660
Management and the Arts 510
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
Positive Obsession: The Life and Times of Octavia E. Butler 500
Surgical Ergonomic Pilot Study Using a Posture Biofeedback Device in Rhinology: A MultiPhase Quality Improvement Study 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7690997
求助须知:如何正确求助?哪些是违规求助? 9252715
关于积分的说明 19978060
捐赠科研通 7263675
什么是DOI,文献DOI怎么找? 3290740
关于科研通互助平台的介绍 2447231
邀请新用户注册赠送积分活动 2295870