实验性自身免疫性肌炎动物模型制作

Establishment of the animal model of experimental autoimmune myositis

目的研究实验性自身免疫性肌炎动物模型的制作方法。方法将实验用SD大鼠分为A(对照组),B(常用剂量组),C(加大剂量组)。采用豚鼠骨骼肌的肌匀浆球蛋白加完全弗氏佐剂(含卡介苗)以不同浓度多次免疫各组大鼠。制成实验性多发性肌炎的模型,观察其临床表现、肌电图、肌酶谱、磁共振及骨骼肌、心肌和肺的病理改变。结果C组症状出现较B组早且重,肌酶谱升高更显著;模型组肌电图均有肌源性损害表现;磁共振检查B组和C组选送标本中各有1只阳性改变;B组有11只,C组全部大鼠骨骼肌出现病理改变,随机选送的心肌标本中有3只阳性改变,肺标本中有1只阳性改变。结论免疫机制与多发性肌炎发病有关;适当加大抗原免疫剂量可以获得更为典型的动物模型。

Objective To find out a method for establishing the animal model of experimental autoirnrnune myositis. Methods SD rats were divided 3 groups of control（A） normal dose（B） and large dose model group（C）. The animal model of experimental polymyositis was induced by repeatedly immunizing the three groups of rats with guinea pig skeletal muscle homogenates added to Freund＇ s complete adjuvant （CFA） （containing BCG vaccine）. The clinical presentations, electromyogram, serum muscle enzymes, MRI, pathology of cardiac muscle and lung were observed. Results Group C had the symptoms earlier and more severe than group B. The serum enzymes in group C increased significantly compared with those in the other groups. Sarcous harmfulness was seen on electromyogram in model groups. MRI showed positive change in one rat of group B and in one rat of group C. Skeletal muscles taken from group C and 11 rats of group B had pathological changes. Three random cardiac muscle samples had positive changes, and positive change was seen in one lung sample. Conclusion Immunity mechanism is related to polymyositis. A better classical animal model may be established by properly increase of antigen immunity dosage.