Bolton C, Flower R J
Pharmacology Group, University of Bath, U.K.
Life Sci. 1989;45(1):97-104. doi: 10.1016/0024-3205(89)90441-4.
Lewis rats, sensitised for the autoimmune condition EAE received a range of doses of the steroid dexamethasone at various times post-inoculation in an attempt to modify the clinical course of the disease. Depending upon the dosing regime employed microgram quantities of the steroid were sufficient to significantly inhibit the clinical development of EAE and milligram doses of the drug completely suppressed the emergence of disease. Administration of the potent anti-glucocorticoid RU38486 to sensitised animals intensified the clinical course of EAE and reversed the steroid-induced inhibition of the disease. Furthermore, after the characteristic loss of neurological symptoms in rats receiving dexamethasone and RU38486, readministration of the anti-glucocorticoid resulted in clinical relapses in the majority of animals. The study emphasises the potent effects of exogenous, physiologically relevant doses of steroid on the course of EAE and, as a result of the observations made using RU38486, considers the role of endogenous steroids in the control of the disease in the rat.
为自身免疫性疾病实验性自身免疫性脑脊髓炎（EAE）致敏的刘易斯大鼠在接种后的不同时间接受了一系列剂量的类固醇地塞米松，试图改变疾病的临床进程。根据所采用的给药方案，微克量的类固醇足以显著抑制EAE的临床发展，而毫克剂量的药物则完全抑制了疾病的出现。向致敏动物施用强效抗糖皮质激素RU38486会加剧EAE的临床进程，并逆转类固醇诱导的疾病抑制作用。此外，在接受地塞米松和RU38486的大鼠出现典型的神经症状消失后，再次施用抗糖皮质激素导致大多数动物出现临床复发。该研究强调了生理相关剂量的外源性类固醇对EAE病程的强效作用，并且由于使用RU38486所做的观察，探讨了内源性类固醇在大鼠疾病控制中的作用。
