抗炎糖皮质激素对人纤维肉瘤细胞和滑膜成纤维细胞中尿激酶型纤溶酶原激活剂mRNA水平的抑制作用。

Medcalf R L, Richards R I, Crawford R J, Hamilton J A

EMBO J. 1986 Sep;5(9):2217-22. doi: 10.1002/j.1460-2075.1986.tb04487.x.

Suppression of plasminogen activator (PA) activity has been invoked as being part of the general anti-inflammatory action of glucocorticoids. Low concentrations of the synthetic glucocorticoid, dexamethasone (Dex), reduce urokinase-type PA mRNA levels in two cell types, namely a human fibrosarcoma line, HT1080, and synovial fibroblast-like cells isolated from human joints. Conversely, metallothionein IIa (MTIIa) mRNA levels in these cells are raised by Dex. These findings, by suggesting that it is possible to suppress urokinase-type PA activity at the level of gene expression, may have therapeutic implications for diseases such as rheumatoid arthritis where proteases may be contributing to the extensive tissue damage and inflammation.

纤溶酶原激活剂（PA）活性的抑制被认为是糖皮质激素一般抗炎作用的一部分。低浓度的合成糖皮质激素地塞米松（Dex）可降低两种细胞类型中尿激酶型PA的mRNA水平，这两种细胞类型分别是人纤维肉瘤细胞系HT1080和从人关节分离出的滑膜成纤维样细胞。相反，这些细胞中的金属硫蛋白IIa（MTIIa）mRNA水平会因Dex而升高。这些发现表明有可能在基因表达水平上抑制尿激酶型PA的活性，这可能对类风湿性关节炎等疾病具有治疗意义，在这些疾病中蛋白酶可能导致广泛的组织损伤和炎症。