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密蒙花通过抑制核因子-κB 和 p38 MAPK 信号通路发挥抗神经炎症活性。

Bridelia ferruginea Produces Antineuroinflammatory Activity through Inhibition of Nuclear Factor-kappa B and p38 MAPK Signalling.

机构信息

Division of Pharmacy and Pharmaceutical Science, Department of Chemical and Biological Sciences, University of Huddersfield, Queensgate, Huddersfield HD1 3DH, UK ; Neurochemistry Research Laboratory, Department of Psychiatry and Psychotherapy, University of Freiburg Medical School, Hauptstraße 5, 79104 Freiburg, Germany.

出版信息

Evid Based Complement Alternat Med. 2012;2012:546873. doi: 10.1155/2012/546873. Epub 2012 Dec 18.

DOI:10.1155/2012/546873
PMID:23320030
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3536297/
Abstract

Bridelia ferruginea is commonly used in traditional African medicine (TAM) for treating various inflammatory conditions. Extracts from the plant have been shown to exhibit anti-inflammatory property in a number of in vivo models. In this study the influence of B. ferruginea (BFE) on the production of PGE(2), nitrite, and proinflammatory cytokines from LPS-stimulated BV-2 microglia was investigated. The effects of BFE on cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expressions were evaluated in LPS-activated rat primary microglia. The roles of NF-κB and MAPK signalling in the actions of BFE were also investigated. BFE (25-200 μg) inhibited the production of PGE(2), nitrite, tumour necrosis factor-α (TNFα), and interleukin-6 (IL-6) as well as COX-2 and iNOS protein expressions in LPS-activated microglial cells. Further studies to elucidate the mechanism of anti-inflammatory action of BFE revealed interference with nuclear translocation of NF-κBp65 through mechanisms involving inhibition of IκB degradation. BFE prevented phosphorylation of p38, but not p42/44 or JNK MAPK. It is suggested that Bridelia ferruginea produces anti-inflammatory action through mechanisms involving p38 MAPK and NF-κB signalling.

摘要

铁仔是一种在传统非洲医学中被广泛使用的植物,用于治疗各种炎症性疾病。该植物的提取物已被证明在许多体内模型中具有抗炎特性。在这项研究中,研究了铁仔(BFE)对 LPS 刺激的 BV-2 小胶质细胞产生 PGE(2)、亚硝酸盐和促炎细胞因子的影响。评估了 BFE 对 LPS 激活的大鼠原代小胶质细胞中环氧化酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)蛋白表达的影响。还研究了 NF-κB 和 MAPK 信号通路在 BFE 作用中的作用。BFE(25-200μg)抑制 LPS 激活的小胶质细胞中 PGE(2)、亚硝酸盐、肿瘤坏死因子-α(TNFα)和白细胞介素-6(IL-6)的产生以及 COX-2 和 iNOS 蛋白表达。进一步阐明 BFE 抗炎作用的机制的研究表明,通过抑制 IκB 降解的机制,干扰 NF-κBp65 的核易位。BFE 阻止了 p38 的磷酸化,但不阻止 p42/44 或 JNK MAPK。因此,Bridelia ferruginea 通过 p38 MAPK 和 NF-κB 信号通路产生抗炎作用。

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