Kurihara A, Ohuchi K, Tsurufuji S
Eur J Pharmacol. 1984 May 18;101(1-2):11-6. doi: 10.1016/0014-2999(84)90025-6.
Using an experimental model for allergic inflammation of the air pouch type in rats, the effects of dexamethasone and indomethacin on leukocyte infiltration and level of chemotactic activity in the inflammatory exudate were examined to clarify the mechanisms of anti-inflammatory effects of glucocorticoids. Both dexamethasone and indomethacin when locally administered inhibited leukocyte infiltration, while chemotactic activity of the exudate was reduced by dexamethasone only. Indomethacin failed to reduce the level of chemotactic activity. Suppression by dexamethasone of the level of chemotactic activity became evident prior to the decrease in the number of leukocytes in the inflammatory exudate. These results suggest that the anti-inflammatory steroids manifest their inhibitory effect on leukocyte infiltration by inhibiting the generation of chemotactic factors in the inflammatory site. Besides this, the possible production of some inhibitory factors by the steroids may be considered as an alternative mechanism.
利用大鼠气囊型过敏性炎症的实验模型,研究了地塞米松和吲哚美辛对炎症渗出物中白细胞浸润和趋化活性水平的影响,以阐明糖皮质激素的抗炎作用机制。地塞米松和吲哚美辛局部给药时均能抑制白细胞浸润,但只有地塞米松能降低渗出物的趋化活性。吲哚美辛未能降低趋化活性水平。地塞米松对趋化活性水平的抑制在炎症渗出物中白细胞数量减少之前就已明显。这些结果表明,抗炎类固醇通过抑制炎症部位趋化因子的产生,对白细胞浸润表现出抑制作用。除此之外,类固醇可能产生一些抑制因子也可被视为一种替代机制。