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芒果苷通过激活核因子红细胞 2 相关因子通路来保护 SOD1-G93A 诱导的 NSC-34 运动神经元免受氧化应激和细胞凋亡。

Mangiferin activates the nuclear factor erythroid 2-related factor pathway to protect SOD1-G93A induced NSC-34 motor neurons from oxidative stress and apoptosis.

机构信息

Medical School of Chinese PLA, Beijing, China.

Neurological Department of the First Medical Center, Chinese PLA General Hospital, Beijing, China.

出版信息

J Biochem Mol Toxicol. 2024 Oct;38(10):e23849. doi: 10.1002/jbt.23849.

DOI:10.1002/jbt.23849
PMID:39264833
Abstract

One of the main factors in the pathophysiology of amyotrophic lateral sclerosis is oxidative stress. Mangiferin (MF), a natural plant polyphenol, has anti-inflammatory and antioxidant effects. The aim of our study was to investigate the protective effects and mechanisms of MF in the hSOD1-G93A ALS cell model. Our result revealed that MF treatment reduced the generation of reactive oxygen species (ROS) and malondialdehyde (MDA), decreased oxidative damage, and reduced apoptosis. Additionally, it was observed that MF significantly increased the synthesis of the antioxidant genes hemeoxygenase-1 and NAD(P)H: quinone oxidoreductase 1, which are downstream of the Nrf2 signaling pathway, and increased the expression and activation of nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 knockdown greatly promoted apoptosis, which was reversed by MF treatment. To summarize, MF promoted the Nrf2 pathway and scavenged MDA and ROS to protect the ALS cell model.

摘要

肌萎缩侧索硬化症的病理生理学的主要因素之一是氧化应激。芒果苷(MF),一种天然植物多酚,具有抗炎和抗氧化作用。我们的研究旨在探讨 MF 在 hSOD1-G93A ALS 细胞模型中的保护作用和机制。我们的结果表明,MF 处理可减少活性氧(ROS)和丙二醛(MDA)的产生,降低氧化损伤,减少细胞凋亡。此外,还观察到 MF 显著增加了抗氧化基因血红素加氧酶-1 和 NAD(P)H:醌氧化还原酶 1 的合成,这是 Nrf2 信号通路的下游,并且增加了核因子红细胞 2 相关因子 2(Nrf2)的表达和激活。Nrf2 敲低显著促进细胞凋亡,而 MF 处理则逆转了这一现象。总之,MF 通过促进 Nrf2 通路并清除 MDA 和 ROS 来保护 ALS 细胞模型。

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