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大麻黄酮A抑制人巨噬细胞中TLR4诱导的趋化因子和细胞因子表达。

Cannflavin A inhibits TLR4-induced chemokine and cytokine expression in human macrophages.

作者信息

Fitzpatrick John-Mark K, O'Riordan Diarmuid, Downer Eric J

机构信息

Discipline of Physiology, School of Medicine, Trinity Biomedical Sciences Institute, Trinity College Dublin, University of Dublin, Dublin, Ireland.

CB1 Botanicals Ltd, Cork, Ireland.

出版信息

Nat Prod Res. 2024 May 23:1-7. doi: 10.1080/14786419.2024.2358382.

Abstract

Cannflavin A (CFL-A), a flavonoid present in the hemp plant L. (), has anti-inflammatory and neuroprotective capacity. Research continues to elucidate the anti-inflammatory effects of components of , with evidence that plant-derived cannabinoids and terpenes can mediate anti-inflammatory activity by targeting toll-like receptor (TLR) signalling, the sensors of pathogen-associated molecules. This study set out to determine if TLR-mediated inflammatory signalling is a CFL-A target using the endotoxin lipopolysaccharide (LPS) to induce TLR4 signalling in human THP-1-derived macrophages. TLR4 activation promoted the production of the chemokine CXCL10 and cytokines IL-1β and TNFα. Treatment with CFL-A dose-dependently attenuated TLR4-induced CXCL10 and IL-1β secretion, with our findings also indicating that the inhibitory effects of CFL-A on chemokine/cytokine secretion are in line with an NF-κB inhibitor. This study highlights TLR4 signalling as a cannflavin target in macrophages.

摘要

大麻黄酮A(CFL-A)是一种存在于大麻植物(L.)中的黄酮类化合物,具有抗炎和神经保护能力。研究不断阐明大麻植物成分的抗炎作用,有证据表明植物来源的大麻素和萜类化合物可通过靶向病原体相关分子的传感器——Toll样受体(TLR)信号通路来介导抗炎活性。本研究旨在使用内毒素脂多糖(LPS)在人THP-1来源的巨噬细胞中诱导TLR4信号通路,以确定TLR介导的炎症信号通路是否是CFL-A的作用靶点。TLR4激活促进了趋化因子CXCL10以及细胞因子IL-1β和TNFα的产生。用CFL-A处理可剂量依赖性地减弱TLR4诱导的CXCL10和IL-1β分泌,我们的研究结果还表明CFL-A对趋化因子/细胞因子分泌的抑制作用与NF-κB抑制剂一致。本研究突出了TLR4信号通路作为巨噬细胞中大麻黄酮的作用靶点。

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