ty-jour t1 - 二甲基umarate抑制cxcl10 通过丙氧氧酶-1在气道平滑肌jf - 欧洲呼吸杂志jo - eur reshir j sp - 195 lp - 202 do - 10.1183 / 09031936.00068411 vl - 41是 -1 Au - Seidel，Petra Au - Coreetler，Katrin E. Au - Hughes，J.Margaret Au - Tamm，Michael Au - Roth，Michael 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道平滑肌束中，从而激活细胞因子分泌和气道平滑肌细胞（ASMC）增殖。二甲基核（DMF）通过淋巴细胞和ASMC通过碘氧酶（HO）-1减少细胞因子分泌。因此，我们研究了DMF抑制肿瘤坏死因子（TNF）-α-和干扰素（IFN）-γ-γ诱导的CXCL10分泌物的致力于人ASMC。在用IFN-γ和/或TNF-α刺激细胞之前，用DMF和/或氟酮和/或谷胱甘肽乙酯预孵育人的原发性ASMC。DMF抑制CXCL10分泌和增加的HO-1水平，P38丝裂原活化蛋白激酶（MAPK）抑制还原DMF依赖性HO-1表达。通过用HO-1小干扰RNA（siRNA）预处理消除了对CXCL10分泌的DMF效应。谷胱甘肽补充逆转所有DMF对CXCL10分泌和P38 MAPK磷酸化的影响。重要的是，将DMF与氟替卡松结合进一步减少CXCL10分泌。 In addition, DMF inhibited IFN-γ-induced CXCL10 secretion. 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 -