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槲皮素和儿茶素通过抑制 TLR4-MyD88 介导的 NF-κB 和 MAPK 信号通路的激活发挥协同抗炎作用。

Synergistic anti-inflammatory effects of quercetin and catechin via inhibiting activation of TLR4-MyD88-mediated NF-κB and MAPK signaling pathways.

机构信息

Key Laboratory of Food Processing Technology and Quality Control in Shandong Province, College of Food Science and Engineering, Shandong Agricultural University, Tai'an, China.

Center of Bee Industry on Seed-Breeding and Popularization in Shandong Province, Tai'an, China.

出版信息

Phytother Res. 2019 Mar;33(3):756-767. doi: 10.1002/ptr.6268. Epub 2019 Jan 14.

DOI:10.1002/ptr.6268
PMID:30637814
Abstract

The synergistic anti-inflammatory effect of quercetin and catechin was investigated using lipopolysaccharide (LPS)-stimulated macrophage RAW 264.7 cells. Results showed that the combined treatment of quercetin with catechin synergistically attenuated LPS-stimulated increase of some proinflammatory molecules, including nitric oxide, tumor necrosis factor α, interleukin-1β, nitric oxide synthase, and cyclooxygenase-2. Moreover, it exhibited significantly (p < 0.05) stronger inhibitory effect on nuclear translocation of nuclear factor-κB (NF-κB) by suppressing the phosphorylation of NF-κB p65 and p50 submits and on the phosphorylation of ETS domain-containing protein and c-Jun N-terminal kinase than any of quercetin or catechin alone. Besides, the cotreatment of quercetin with catechin significantly (p < 0.05) restored the impaired expression of toll-like receptor 4, myeloid differentiation primary response gene 88, and some downstream effectors (IRAK1, TRAF6, and TAK1). These results suggest that quercetin and catechin possessed synergistic anti-inflammatory effects, which may be attributed to their roles in suppressing the activation of TLR4-MyD88-mediated NF-κB and mitogen-activated protein kinases signaling pathways.

摘要

采用脂多糖(LPS)刺激的巨噬细胞 RAW 264.7 细胞研究了槲皮素和儿茶素的协同抗炎作用。结果表明,槲皮素与儿茶素联合处理协同减弱了 LPS 刺激引起的一些促炎分子的增加,包括一氧化氮、肿瘤坏死因子-α、白细胞介素-1β、一氧化氮合酶和环加氧酶-2。此外,它通过抑制 NF-κB p65 和 p50 亚基的磷酸化以及 ETS 结构域包含蛋白和 c-Jun N-末端激酶的磷酸化,对核转录因子-κB(NF-κB)的核易位表现出显著(p<0.05)更强的抑制作用,而单独使用槲皮素或儿茶素则没有。此外,槲皮素与儿茶素的共同处理显著(p<0.05)恢复了 Toll 样受体 4、髓样分化初级反应基因 88 和一些下游效应物(IRAK1、TRAF6 和 TAK1)的表达受损。这些结果表明,槲皮素和儿茶素具有协同的抗炎作用,这可能归因于它们在抑制 TLR4-MyD88 介导的 NF-κB 和丝裂原激活蛋白激酶信号通路的激活中的作用。

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