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鞣酸通过抑制 NF-κB 活化对脂多糖诱导的 BV2 小胶质细胞的抗神经炎症作用。

Anti-neuroinflammatory effects of tannic acid against lipopolysaccharide-induced BV2 microglial cells via inhibition of NF-κB activation.

机构信息

Department of Neurology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.

Department of Neurosurgery, The Second People's Hospital of Yunnan Province, Kunming, Yunnan, China.

出版信息

Drug Dev Res. 2019 Mar;80(2):262-268. doi: 10.1002/ddr.21490. Epub 2019 Feb 6.

DOI:10.1002/ddr.21490
PMID:30724376
Abstract

Microglia mediated neuroinflammation is known to cause various neurodegenerative and neurological ailments. Tannic acid is a natural polyphenol which has been reported to possess antioxidant, anti-inflammatory, anticarcinogenic, antimutagenic, antitumor, and antimicrobial activities. As there are no reports till date on the anti-neuroinflammatory effects of tannic acid, this study was conducted to analyze the possible mechanism and pathway involved in the prevention of neuroinflammation by tannic acid in BV2 microglial cells. BV2 microglial cells were pretreated with tannic acid (10, 25, and 50 μM/mL) and induced with lipopolysaccharide (LPS; 1 μM/mL) to assess the production of reactive oxygen species (ROS), nitric oxide (NO), prostaglandin E2 (PGE2), pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α), and nuclear factor-kappa B (NF-κB) protein expressions through western blotting. The results showed that LPS significantly activated the BV2 cells via toll-like receptor 4 to induce elevated productions of ROS, NO, PGE2, IL-6, and IL-1β. However, tannic acid was able to reverse all the neuroinflammatory effects of LPS-induced BV2 cells in a dose-dependent manner. Collectively, the anti-inflammatory effects of tannic acid on LPS-induced BV2 microglial cells are attributed to the inhibition of ROS formation and the suppression of NF-κB pathway activation. Tannic acid could be a potential therapeutic agent for the treatment of neurological related disorders.

摘要

小胶质细胞介导的神经炎症已知会导致各种神经退行性和神经疾病。单宁酸是一种天然多酚,据报道具有抗氧化、抗炎、抗癌、抗突变、抗肿瘤和抗菌活性。由于迄今为止尚无关于单宁酸的抗神经炎症作用的报道,因此进行了这项研究,以分析单宁酸在 BV2 小胶质细胞中预防神经炎症的可能机制和途径。用单宁酸(10、25 和 50μM/ml)预处理 BV2 小胶质细胞,并诱导脂多糖(LPS;1μM/ml),通过 Western blot 评估活性氧(ROS)、一氧化氮(NO)、前列腺素 E2(PGE2)、促炎细胞因子(IL-6、IL-1β 和 TNF-α)和核因子-κB(NF-κB)蛋白表达的产生。结果表明,LPS 通过 Toll 样受体 4 显著激活 BV2 细胞,诱导 ROS、NO、PGE2、IL-6 和 IL-1β 的产生增加。然而,单宁酸能够以剂量依赖的方式逆转 LPS 诱导的 BV2 细胞的所有神经炎症作用。总之,单宁酸对 LPS 诱导的 BV2 小胶质细胞的抗炎作用归因于抑制 ROS 形成和抑制 NF-κB 途径的激活。单宁酸可能是治疗神经相关疾病的潜在治疗剂。

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