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化合物48/80对Lewis大鼠实验性自身免疫性脑脊髓炎的减轻作用

Attenuation of experimental autoimmune encephalomyelitis by Compound 48/80 in Lewis rats.

作者信息

Stanley N C, Jackson F L, Orr E L

机构信息

Department of Anatomy and Cell Biology, Texas College of Osteopathic Medicine, Fort Worth 76107.

出版信息

J Neuroimmunol. 1990 Sep-Oct;29(1-3):223-8. doi: 10.1016/0165-5728(90)90165-j.

Abstract

The appearance of increased levels of histamine in the central nervous system (CNS) concomitant with the development of clinically significant acute experimental autoimmune encephalomyelitis (EAE) in male Lewis rats suggests that CNS-associated mast cells may mediate acute EAE in Lewis rats. We now report that, compared to controls, rats with acute EAE exhibit fewer detectable mast cells in their dura mater and velum interpositum. In addition, intracisternal, but not intraperitoneal administration of Compound 48/80 just prior to the appearance of clinical signs of acute or recurrent EAE in male and female rats, respectively, significantly attenuates the clinical severity of both forms of EAE. These results further support the hypothesis that CNS-associated, but not peripheral mast cells are mediators or modulators of acute and recurrent EAE in Lewis rats.

摘要

在雄性Lewis大鼠中,随着具有临床意义的急性实验性自身免疫性脑脊髓炎(EAE)的发展,中枢神经系统(CNS)中组胺水平升高,这表明与CNS相关的肥大细胞可能介导Lewis大鼠的急性EAE。我们现在报告,与对照组相比,患有急性EAE的大鼠在其硬脑膜和中间帆中可检测到的肥大细胞较少。此外,分别在雄性和雌性大鼠出现急性或复发性EAE临床症状之前,经脑池内而非腹腔内注射化合物48/80,可显著减轻两种形式EAE的临床严重程度。这些结果进一步支持了以下假设:与CNS相关而非外周肥大细胞是Lewis大鼠急性和复发性EAE的介质或调节因子。

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