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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >5,7-Dihydroxy-3,4,6-trimethoxyflavone inhibits intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 via the Akt and nuclear factor-κB-dependent pathway, leading to suppression of adhesion of monocytes and eosinophils to bronchial epithelial cells
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5,7-Dihydroxy-3,4,6-trimethoxyflavone inhibits intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 via the Akt and nuclear factor-κB-dependent pathway, leading to suppression of adhesion of monocytes and eosinophils to bronchial epithelial cells

机译：5,7-二羟基-3,4,6-三甲氧基黄酮通过Akt和核因子-κB依赖性途径抑制细胞间黏附分子1和血管细胞黏附分子1，从而抑制单核细胞和嗜酸性粒细胞与支气管上皮细胞的黏附

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摘要

5,7-Dihydroxy-3′,4′,6′-trimethoxyflavone (eupatilin), the active pharmacological ingredient from Artemisia asiatica Nakai (Asteraceae), is reported to have a variety of anti-inflammatory properties in intestinal epithelial cells. However, little information is known about the molecular mechanism of eupatilin-induced attenuation of bronchial epithelial inflammation. This study investigates the role of eupatilin in the adhesion of inflammatory cells such as monocytes and eosinophils to bronchial epithelial cells. Stimulation of a human bronchial epithelial cell line (BEAS-2B) with tumour necrosis factor-α (TNF-α) increased the expression of surface adhesion molecules, including intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), in which eupatilin significantly inhibited the expression of those adhesion molecules in a dose-dependent manner. Eupatilin suppressed the TNF-α-induced activation of IκBα and nuclear factor-κB (NF-κB) signals in BEAS-2B cells. The IκB kinase (IKK) activation was also significantly reduced in eupatilin-pre-treated BEAS-2B and primary normal human bronchial epithelial (NHBE) cells. However, eupatilin did not influence AP-1 activity in TNF-α-stimulated cells. Suppression of NF-κB signalling induced by eupatilin resulted in the inhibition of the expression of adhesion molecules and the adhesion of monocytes and eosinophils to BEAS-2B cells. Furthermore, eupatilin suppressed the phosphorylation of Akt in TNF-α-stimulated BEAS-2B and NHBE cells, leading to down-regulation of NF-κB activation and adhesion molecule expression and finally to suppression of the inflammatory cell adhesion to epithelial cells. These results suggest that eupatilin can inhibit the adhesion of inflammatory cells to bronchial epithelial cells via a signalling pathway, including activation of Akt and NF-κB, as well as expression of adhesion molecules.
机译：据报道，来自Artemisia asiatica Nakai（菊科）的活性药理成分5,7-二羟基-3'，4'，6'-三甲氧基黄酮（依帕替林）在肠上皮细胞中具有多种抗炎特性。然而，关于紫杉醇诱导的支气管上皮炎症减轻的分子机制的信息知之甚少。这项研究调查了依帕替林在炎性细胞（如单核细胞和嗜酸性粒细胞）与支气管上皮细胞粘附中的作用。用肿瘤坏死因子-α（TNF-α）刺激人支气管上皮细胞系（BEAS-2B）可以增加表面粘附分子的表达，包括细胞间粘附分子1（ICAM-1）和血管细胞粘附分子1（VCAM） -1），其中依帕替林以剂量依赖性方式显着抑制那些粘附分子的表达。依匹帕林抑制BEAS-2B细胞中TNF-α诱导的IκBα和核因子-κB（NF-κB）信号的激活。 Eupatilin预处理的BEAS-2B和原代正常人支气管上皮（NHBE）细胞中的IκB激酶（IKK）活化也显着降低。然而，依帕替林并不影响TNF-α刺激的细胞中AP-1的活性。依帕替林诱导的NF-κB信号转导的抑制导致粘附分子表达的抑制以及单核细胞和嗜酸性粒细胞对BEAS-2B细胞的粘附。此外，依法帕林抑制TNF-α刺激的BEAS-2B和NHBE细胞中Akt的磷酸化，导致NF-κB活化和粘附分子表达下调，并最终抑制炎性细胞粘附于上皮细胞。这些结果表明，依帕替林可通过信号传导途径抑制炎症细胞对支气管上皮细胞的粘附，包括激活Akt和NF-κB以及粘附分子的表达。

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