Epigallocatechin-3-gallate Inhibits LPS/AβO-induced Neuroinflammation in BV2 Cells through Regulating the ROS/TXNIP/NLRP3 Pathway.

Yanyan Xiao, Chenglin Yang, Nana Si, Tao Chu, Jiahui Yu, Xintong Yuan, Xiang-Tao Chen
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Abstract

Neuroinflammation is a key factor in cognitive dysfunction and neurodegenerative diseases such as Alzheimer's disease (AD), so inhibiting neuroinflammation is considered as a potential treatment for AD. Epigallocatechin-3-gallate (EGCG), a polyhydroxyphenol of green tea, has been found to exhibit anti-oxidative, anti-inflammatory and neuroprotective effects. The aim of this study was to investigate the inhibitory effect of EGCG on inflammation and its mechanism. In this study, BV2 cells were simultaneously exposed to lipopolysaccharides (LPS) and the amyloid-β oligomer (AβO) to induce inflammatory microenvironments. Inflammatory cytokines and NLRP3 inflammasome-related molecules were detected by RT-PCR and Western Blot. The results show that EGCG inhibits LPS/AβO-induced inflammation in BV2 cells through regulating IL-1β, IL-6, and TNF-α. Meanwhile, EGCG reduces the activation of the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome and levels of intracellular ROS in BV2 cells treated with LPS/AβO by affecting the mitochondrial membrane potential (MMP). Further research found that EGCG inhibited MMP through regulating thioredoxin-interacting protein (TXNIP) in LPS/AβO-induced neuroinflammation. In conclusion, EGCG may alleviate LPS/AβO-induced microglial neuroinflammation by suppressing the ROS/ TXNIP/ NLRP3 pathway. It may provide a potential mechanism underlying the anti-inflammatory properties of EGCG for alleviating AD.

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表没食子儿茶素-3-棓酸盐通过调节 ROS/TXNIP/NLRP3 通路抑制 LPS/AβO 诱导的 BV2 细胞神经炎症
神经炎症是认知功能障碍和阿尔茨海默病(AD)等神经退行性疾病的关键因素,因此抑制神经炎症被认为是治疗阿尔茨海默病的潜在方法。表没食子儿茶素-3-棓酸盐(EGCG)是绿茶中的一种多羟基酚,具有抗氧化、抗炎和保护神经的作用。本研究旨在探讨 EGCG 对炎症的抑制作用及其机制。在这项研究中,BV2 细胞同时暴露于脂多糖(LPS)和淀粉样β寡聚体(AβO),以诱导炎症微环境。通过 RT-PCR 和 Western Blot 检测炎性细胞因子和 NLRP3 炎性体相关分子。结果表明,EGCG 可通过调节 IL-1β、IL-6 和 TNF-α 抑制 LPS/AβO 诱导的 BV2 细胞炎症。同时,EGCG通过影响线粒体膜电位(MMP),降低了NOD-、LRR-和含吡咯啉结构域蛋白3(NLRP3)炎性组的活化,并降低了经LPS/AβO处理的BV2细胞的细胞内ROS水平。进一步的研究发现,在 LPS/AβO 诱导的神经炎症中,EGCG 通过调节硫氧还蛋白相互作用蛋白(TXNIP)来抑制 MMP。总之,EGCG可通过抑制ROS/ TXNIP/ NLRP3通路缓解LPS/AβO诱导的小胶质细胞神经炎症。这可能为EGCG缓解AD的抗炎特性提供了潜在机制。
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