TY -的T1 Dimethylfumarate抑制CXCL10通过< / em > < em >血红素在气道平滑肌oxygenase-1 JF -欧洲呼吸杂志》乔和J SP - 195 LP - 202欧元做- 10.1183/09031936.00068411六世- 41 - 1 AU -佩特拉塞德尔盟凯特琳·e·Hostettler AU - J·玛格丽特·休斯AU -迈克尔·塔姆AU -迈克尔·罗斯Y1 - 2013/01/01 UR - //www.qdcxjkg.com/content/41/1/195.abstract N2 - CXCL10刺激肥大细胞浸润到气管平滑肌束,因此,激活细胞因子分泌和气道平滑肌细胞(ASMC)扩散。Dimethylfumarate (DMF)减少淋巴细胞分泌的细胞因子和ASMC增殖通过血红素氧合酶(HO) 1。因此,我们调查的效力DMF抑制肿瘤坏死因子(TNF) -α-和干扰素(IFN) -γ-induced CXCL10分泌人体asmc。人类基本的asmc pre-incubated DMF和/或和/或谷胱甘肽ethylester之前与IFN-γ和/或TNF-α细胞被刺激。DMF抑制CXCL10分泌和增加HO-1水平和p38增殖蛋白激酶(MAPK)抑制减少DMF-dependent HO-1表达式。DMF对CXCL10分泌的影响被预处理废除HO-1小干扰RNA (siRNA)。谷胱甘肽补充了所有DMF对CXCL10分泌和p38 MAPK磷酸化的影响。重要的是,进一步结合DMF卡松CXCL10分泌减少。此外,DMF抑制IFN-γ-induced CXCL10分泌。这种效应被补充谷胱甘肽或补偿与HO-1 siRNA预处理。 In addition, DMF reduced TNF-α-induced granulocyte colony-stimulating factor (G-CSF) secretion but had no effect on INF-γ-induced G-CSF secretion. In human primary ASMCs, DMF inhibits CXCL10 secretion by reducing the cellular glutathione level and by activation of p38 MAPK and HO-1. Therefore, DMF may reduce airway inflammation in asthma by a glucocorticoid-independent pathway. ER -