Role of Nrf2 Pathway Activation in Neurological Disorder: A Brief Review

IF 0.4 Q4 PHARMACOLOGY & PHARMACY Journal of Pharmacology & Pharmacotherapeutics Pub Date : 2022-09-01 DOI:10.1177/0976500X221128855
Mohammad Zubair Baba, S. Gomathy, Umair Wahedi
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引用次数: 1

Abstract

Oxidative stress plays a crucial role in the emergence of numerous neurodegenerative diseases, with protein accumulation and mitochondrial damage, which result in neurological disorders. To minimize oxidative stress, several defensive mechanisms protect nerve cells by releasing antioxidants such as nuclear erythroid factor2 (Nrf2)-Kelch-like ECH-associated protein1 (Keap1) signaling pathway activation has been proved to be a prospective treatment to reduce oxidative stress and neuroinflammation for protection of neurons in a variety of neurological disorders. In this review, we focus beneficial role of Nrf2 in Alzheimer’s and Parkinson’s diseases. Nrf2 is proved to be a master regulator of antioxidants by releasing over 250 cytoprotective genes aimed at oxidative stress and neuroinflammation. In animal studies Nrf2 activation is proved to improve autophagy, mitochondrial biogenesis, and Suppression of inflammatory cytokinin which protects neuronal cells and inhibit progressive neurodegeneration.
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Nrf2通路激活在神经系统疾病中的作用:综述
氧化应激在许多神经退行性疾病的出现中起着至关重要的作用,蛋白质积累和线粒体损伤会导致神经系统疾病。为了最大限度地减少氧化应激,几种防御机制通过释放抗氧化剂来保护神经细胞,如核红细胞因子2(Nrf2)-凯尔奇样ECH相关蛋白1(Keap1)信号通路激活已被证明是一种减少氧化应激和神经炎症的前瞻性治疗方法,用于保护各种神经疾病中的神经元。在这篇综述中,我们关注Nrf2在阿尔茨海默病和帕金森病中的有益作用。Nrf2通过释放250多个针对氧化应激和神经炎症的细胞保护基因,被证明是抗氧化剂的主要调节因子。在动物研究中,Nrf2的激活被证明可以改善自噬、线粒体生物发生和抑制炎性细胞分裂素,后者保护神经元细胞并抑制进行性神经退行性变。
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来源期刊
CiteScore
0.40
自引率
0.00%
发文量
37
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