TY -的T1 Dimethylfumarate抑制CXCL10通过< / em > < em >血红素oxygenase-1气管平滑肌JF -欧洲呼吸杂志乔-欧元和J SP - 195 LP - 202——10.1183/09031936.00068411六世- 41 - 1 AU -塞德尔,佩特拉盟——Hostettler,凯特琳e . AU -休斯,J .玛格丽特AU -塔姆,迈克尔AU -罗斯,N2 - CXCL10刺激肥大细胞渗入气道平滑肌束，从而激活细胞因子分泌和气道平滑肌细胞(ASMC)增殖。富马酸二甲基(DMF)通过血红素加氧酶(HO)-1减少淋巴细胞分泌细胞因子和ASMC增殖。因此，我们研究了DMF对人ASMCs分泌肿瘤坏死因子(TNF)-α-和干扰素(IFN)-γ-诱导CXCL10的抑制作用。人初级ASMCs用DMF和/或氟替卡松和谷胱甘肽乙酯预孵育，然后用IFN-γ和/或TNF-α刺激细胞。DMF抑制CXCL10分泌并增加HO-1水平，抑制p38促丝分裂原活化蛋白激酶(MAPK)降低DMF依赖的HO-1表达。HO-1小干扰RNA (siRNA)预处理可消除DMF对CXCL10分泌的影响。补充谷胱甘肽逆转了DMF对CXCL10分泌和p38 MAPK磷酸化的所有影响。重要的是，DMF与氟替卡松联合使用进一步降低了CXCL10的分泌。此外，DMF抑制IFN-γ诱导的CXCL10分泌。 This effect was compensated by glutathione supplementation or by pre-treatment with HO-1 siRNA. 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 -