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糖皮质激素受体阻断对大鼠实验性自身免疫性重症肌无力的影响
引用本文:蒋建明,涂来慧.糖皮质激素受体阻断对大鼠实验性自身免疫性重症肌无力的影响[J].中华神经科杂志,1997,30(2):77-80.
作者姓名:蒋建明  涂来慧
作者单位:第二军医大学长海医院神经科
摘    要:研究重症肌无力(MG)患者外周血白细胞糖皮质激素受体(GR)减少,而血浆皮质醇则在正常范围,探讨其与MG发病的关系。方法SD大鼠32只,随机分成4组。实验组先以GR的竞争性拮抗剂米非司酮(RU38486,RU486)阻断其GR,再以从人肌肉中粗提的乙酰胆碱受体(nAChR)进行免疫;实验对照组单用nAChR,试剂对照组只用RU486,而正常对照组仅用福氏佐剂。以临床症状、血清抗nAChR抗体(nAChR-ab),重复刺激坐骨神经递减幅度为观察指标。结果实验组的临床症状和nAChR-ab滴度升高及肌电图递减幅度均较明显,经t检验分析,均与实验对照组有显著性差异(P<0.05),而试剂对照组和正常对照组均无MG的表现。结论GR被阻断后,对大鼠的实验性自身免疫性MG(EAMG)发病有易化作用。

关 键 词:重症肌无力  受体.糖皮质激素  抗体.乙酰胆碱受体  肌电图

Effect of blockage of glucocorticoid receptor on experimental autoimmune myasthenia gravis in rats
Jiang Jianming,Tu Laihui,Zhang Renqin,et al..Effect of blockage of glucocorticoid receptor on experimental autoimmune myasthenia gravis in rats[J].Chinese Journal of Neurology,1997,30(2):77-80.
Authors:Jiang Jianming  Tu Laihui  Zhang Renqin  
Institution:Jiang Jianming,Tu Laihui,Zhang Renqin,et al. Department of Neurology,Changhai Hospital,Second Military Medical University,Shanghai 200433
Abstract:Objective Our previous clinical studies have shown that the glucocorticoid receptors (GR) of the leukocytes in peripheral blood of myasthenia gravis (MG) patients are lessened, while the plasma concentration of cortisol is normal. From these, we presume that there may be some relation between the lessening of GR and the onset of MG. Method Therefore, we used 32 Spraque Dauley(SD) rats and divided them into four groups at random. In the experimental group, after the GR blocked by RU 38 486(RU 486), the rats were immunized repeated with the crude extract of human muscle acetylcholine receptor (AChR). The experimental controls were only immuniced repeatedly with AChR. The reagent controls were only injected with RU 486, while the normal controls were injected only with the adjuvants. We observed the clinical symptoms of the rats, the titors of AChR Antibody (AChR ab) and the degrees of decremental responses to repeated stimulations of the sciatic nerves. Results Experimental rats had significantly more serious muscular weakness, higher titers of AChR ab, and more decremental response to repeated stimul on the sciatic nerves than these of the experimental controls. It has a remarkable difference by t test ( P <0.05). While both the reagent controls and the normal controls have no symptoms of MG. Conclusions It suggests that the lessening of GR play a facilitatory role to the onset of experimental autoimmune myasthenia gravis (EAMG).
Keywords:Myasthenia gravis    Glucocorticoid receptor    Acetylcholine receptor    Electromyogram
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