Goodman R, Stevens T M, Mantegna L R, Kidd P R, Harris R R, Kerr J S
Du Pont Merck Pharmaceutical Company, Wilmington, DE 19898.
Agents Actions. 1991 Sep;34(1-2):113-6. doi: 10.1007/BF01993253.
We have investigated the role of recombinant human interleukin-1 beta (rIL-1 beta) and recombinant human tumor necrosis factor alpha (rTNF-alpha) on PLA2 activity, protein synthesis and eicosanoid production in bovine pulmonary artery endothelial cells. Cellular PLA2 activity increased 4-fold and production of PGE2 increased 3-fold at 1-2 hrs in the presence of 10 units/ml rIL-1 beta. PLA2 activity increased 3-fold at 30 min and PGE2 production increased 2-fold with 5 x 10(-9) M rTNF-alpha. The data show that endothelial cells respond more rapidly to rIL-1 beta (2-6 hr) and rTNF-alpha (30 min) than do chondrocytes and synovial cells (6-16 hrs), suggesting endothelial cells may play a primary role in initiating the inflammatory response.
我们研究了重组人白细胞介素-1β(rIL-1β)和重组人肿瘤坏死因子α(rTNF-α)对牛肺动脉内皮细胞中磷脂酶A2(PLA2)活性、蛋白质合成和类花生酸生成的作用。在存在10单位/毫升rIL-1β的情况下,细胞PLA2活性在1 - 2小时内增加了4倍,PGE2的生成增加了3倍。在5×10⁻⁹ M rTNF-α作用下,PLA2活性在30分钟时增加了3倍,PGE2生成增加了2倍。数据表明,内皮细胞对rIL-1β(2 - 6小时)和rTNF-α(30分钟)的反应比软骨细胞和滑膜细胞(6 - 16小时)更快,这表明内皮细胞可能在引发炎症反应中起主要作用。