摘要
摘 要：目的 探讨口服髓磷脂碱性蛋白（MBP）治疗实验性自身免疫性神经炎（EAN）的效果。方法 应用牛周围神经 MBP免疫豚鼠建立 EAN动物模型。应用国际分级标准和临床评分对发病豚鼠进行临床评定；对 EAN豚鼠坐骨神经进行常规病理、免疫组化、半薄切片的光镜及电镜观察；剥离单神经纤维，评定其脱髓复髓情况。结果用 MBP建立豚鼠 EAN模型其发病率为 87．5％，免疫诱导的 12～16d出现典型瘫痪症状，高峰期在 14～21d，以后进入恢复阶段。发病高峰期坐骨神经病理为小血管周围大量的淋巴细胞、巨噬细胞浸润，神经纤维肿胀、变性，髓鞘脱失；恢复期神经组织内浸润的细胞明显减少，神经纤维肿胀、脱髓的现象明显减轻，施万细胞明显增生。在发病高峰时开始治疗，口服MBP和腹腔注射静脉用丙种球蛋白（IVIG）治疗均促使豚鼠临床得分提前下降，坐骨神经病理在21d时表现为浸润的淋巴细胞减少，肌髓鞘纤维减少，复髓纤维增多。结论 MBP口服治疗EAN，明显地促进其临床和病理提前恢复，其机制可能是大剂量MBP口服诱导机体免疫耐受的结果。
Abstract: Objective To interprete the effect of myelin basic protein(MBP) inducing the immunetolerance of experimental autoimmune neuritis(EAN). Methods Guinea pigs EAN model was established by MBP. Applying international grade and clinical scores standard,EAN guinea pigs were assesed. Routine pathology,immunocy-tochemistry semi-thin dissection of sciatic nerve were systematically examined under light microscope and electric microscope. The demyelination and the remyelination of single sciatic nerve were assesed. Results The EAN ratio induced by BPM was 87. 5% ,and the onset of typical paralysis was following inducing from 12 to 16days,the peak stage was between 14 and 21 days,then come the remission stage. In the peak stage,the pathologic change of sciatic nerve were infiltrated by lymphocyte and macrophage. The nerve fiber present swelling, dissecting, degeneration. In remission stage,the infiltrating cell decreased signicantly,the swelling and dissecting of nerve fibre alleviated , and schwann cell proliferated predominantly. In the MBP group and the IVIG group, not only the clinical symptom but also neuropathological change restored significantly at 21th day. Single nerve fibers of sciatic nerve showed decreasing demyelination and increasing remyelination. Conclusion Oral BPM treament as well as in-traperitoneal IVIG treatment can amelioated the EAN ,and the mechanism may be that high -dose oral BPM inducing immune tolerance.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2002年第1期26-28,共3页
Journal of Apoplexy and Nervous Diseases
