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地塞米松或环孢素A短期治疗对实验性变应性脑脊髓炎血脑屏障破坏的抑制作用。

Inhibition of blood-brain barrier disruption in experimental allergic encephalomyelitis by short-term therapy with dexamethasone or cyclosporin A.

作者信息

Paul C, Bolton C

机构信息

Pharmacology Group, School of Pharmacy and Pharmacology, University of Bath, U.K.

出版信息

Int J Immunopharmacol. 1995 Jun;17(6):497-503. doi: 10.1016/0192-0561(95)00034-y.

DOI:10.1016/0192-0561(95)00034-y
PMID:7499026
Abstract

Double radioisotope measurement of neurovascular integrity in Lewis rats inoculated for experimental allergic encephalomyelitis (EAE) showed abnormal elevation of albumin extravasation in the cerebellum, medulla-pons and cervical spinal cord at the time of clinical manifestation. Therapeutically administered dexamethasone (Dex) (0.1-1 mg/kg body weight) or cyclosporin A (CsA) (25-75 mg/kg body weight) dose-dependently reduced albumin movement across the blood-brain barrier (BBB). Dex at a dose of 1 mg/kg completely suppressed abnormal BBB permeability in all tissues (P < or = 0.001), while CsA at the highest dose of 75 mg/kg achieved highly significant (P < or = 0.001), but not complete, suppression of aberrant barrier leakage in the areas studied. The implications of these findings to possible drug action at the immunocompromised cerebrovasculature are discussed.

摘要

对接种实验性变态反应性脑脊髓炎(EAE)的Lewis大鼠进行双放射性同位素神经血管完整性测量显示,在临床表现期,小脑、延髓脑桥和颈脊髓中的白蛋白外渗异常升高。治疗性给予地塞米松(Dex)(0.1 - 1mg/kg体重)或环孢素A(CsA)(25 - 75mg/kg体重)可剂量依赖性地减少白蛋白穿过血脑屏障(BBB)的移动。剂量为1mg/kg的Dex完全抑制了所有组织中异常的BBB通透性(P≤0.001),而最高剂量为75mg/kg的CsA对所研究区域异常的屏障渗漏实现了高度显著(P≤0.001)但非完全的抑制。讨论了这些发现对免疫受损脑血管可能的药物作用的影响。

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