Ahluwalia A, Newbold P, Brain S D, Flower R J
Department of Biochemical Pharmacology, William Harvey Research Institute, Medical College of St Bartholomew's Hospital, London, UK.
Eur J Pharmacol. 1995 Sep 5;283(1-3):193-8. doi: 10.1016/0014-2999(95)00350-t.
Topical glucocorticoid treatment (betamethasone-17-valerate (0.018 mg/cm2, 3 h pretreatment) significantly inhibited neurogenic oedema formation induced by electrical antidromic stimulation (2 Hz, 15 V, 0.1 ms for 5 min) of the rat saphenous nerve; a response mediated by neuropeptides released from activated capsaicin-sensitive sensory C-fibres. Oedema formation was estimated by measurement of extravasation of i.v. injected 125I-albumin into skin. The inhibitory effect of the topical glucocorticoid was reversed by passive immunisation of rats with polyclonal antibody to the glucocorticoid-inducible anti-inflammatory protein lipocortin 1 (1 ml/kg, s.c., 24 h pretreatment) whilst a non-immune serum was without effect. Similarly the glucocorticoid receptor antagonist RU38486 (20 mg/kg, 2 and 20 h pretreatment) abrogated the response indicating specific binding to glucocorticoid receptors. Topical glucocorticoid treatment also inhibited the oedema produced by intradermal substance P (0.1 nmol) in the dorsal skin of rats. Topical glucocorticoid inhibited neurogenic oedema formation partly through a mechanism dependent upon lipocortin 1. This inhibition may be partly due to a post-junctional effect upon substance P activity/binding however a pre-junctional component cannot be excluded.
局部糖皮质激素治疗（倍他米松-17-戊酸酯（0.018mg/cm²，预处理3小时）可显著抑制大鼠隐神经电逆向刺激（2Hz，15V，0.1ms，持续5分钟）诱导的神经源性水肿形成；该反应由活化的辣椒素敏感感觉C纤维释放的神经肽介导。通过测量静脉注射的125I-白蛋白向皮肤的外渗来评估水肿形成。用糖皮质激素诱导的抗炎蛋白脂皮质素1的多克隆抗体对大鼠进行被动免疫（1ml/kg，皮下注射，预处理24小时）可逆转局部糖皮质激素的抑制作用，而非免疫血清则无此作用。同样，糖皮质激素受体拮抗剂RU38486（20mg/kg，预处理2小时和20小时）可消除该反应，表明其与糖皮质激素受体特异性结合。局部糖皮质激素治疗还可抑制大鼠背部皮肤皮内注射P物质（0.1nmol）产生的水肿。局部糖皮质激素部分通过依赖脂皮质素1的机制抑制神经源性水肿形成。这种抑制可能部分归因于对P物质活性/结合的接头后效应，不过接头前成分也不能排除。
