摘要
目的采用乙酰胆碱受体(nAChR)单克隆抗体-mAb35建立C57BL/6幼年小鼠重症肌无力被动转移模型(passive transferred myasthen ia gravis,PTMG),摸索成功建立动物模型的mAb35的有效剂量,为进一步探讨重症肌无力(myasthen ia gravis,MG)的发病机制和免疫治疗提供实验动物模型。方法将实验组分为3组(E1、E2、E3),分别经腹腔注射含0.5、1.0、1.5 mg/kg mAb35的R inger’s液0.2m l给B6幼年小鼠,对照组(N)注射不含mAb35的R inger’s液0.2m l。观察其临床表现,并进行药理学、神经电生理学及电镜超微结构鉴定,同时检测血清中nAChRAb水平,以判断模型建立是否成功。结果实验组小鼠表现不同程度的MG临床症状,电生理改变、药理学特征、血清学AChRAb升高及超微结构病理改变等均符合MG的病理生理特点。结论利用AChR单克隆抗体-mAb35可在幼年C57BL/6小鼠成功建立PT-MG模型,其有效剂量为1.0 mg/kg,该方法简便、可靠、敏感,为研究儿童MG提供了一种很好的实验动物模型。
Objective To establish an animal model of passive transferred myasthenia gravis （PTMG） in C57BL/6 mice aged 4 to 5 weeks with nicotinic acetylcholine receptor monoclonal antibody-mAb35 so as to decide the effective dose of mAb35 required to induce PTMG and to supply animal model for further study of the pathogenesis and immunotherapy of human MG. Methods The C57BL/6 mice aged 4 to 5 weeks in the experimental group were divided into three subgroups （ E1, E2, E3 ）, injected intraperitoneally （ i. p. ） with 0.2 ml of Ringer＇s buffer solution containing 0.5, 1.0 or 1.5 mg/kg capital monoclonal antibody mAb35 of acetylcholine receptor respectively. The control group （N） were injected i.p. with 0.2 ml of Ringer＇ s buffer solution without mAb35. To decide whether the model was successful, the clinical symptoms, ultrastructural changes of the mice as well as pharmacological and electrophysiological evaluation were observed and the serum levels of acetylcholine receptor antibody （AChRAb） were detected. Results All mice in the experimental groups were induced of clinic symptoms of myasthenia. The features in pharmacology, electrophysiology, ultrastructure and increased level of acetylcholine receptor antibody were in accordance with those of MG patients. Conclusion The model of PTMG can be successfully induced in C57BL/6 mice with mAb35 at effective dose of 1.0 mg/kg. The method is convenient and reliable. A fine animal model is established for experimental study of myasthenia gravis in children.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2006年第13期1397-1400,共4页
Journal of Third Military Medical University
关键词
重症肌无力
单克隆抗体
被动转移
myasthenia gravis
monoclonal antibody
passive transfer
