实验性自身免疫性肌炎动物模型制作的研究

发布时间：2018-04-01 02:26

本文选题：多发性肌炎　切入点：SD大鼠　出处：《苏州大学》2007年硕士论文

【摘要】： 目的:研究制作实验性自身免疫性肌炎动物模型的方法方法:将实验用SD大鼠分为3组,A组8只为对照组,B组和C组为模型组,B组16只,为常用剂量组,C组16只,为加大剂量组。采用豚鼠骨骼肌的肌匀浆球蛋白(分别为15mg/ml、30mg/ml)加完全弗氏佐剂(含卡介苗)以不同浓度多次免疫各组SD大鼠,A组免疫物为生理盐水加等量的CFA,B组免疫物为15mg/ml的肌匀浆加等量的CFA,C组为30mg/ml的肌匀浆加等量的CFA。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:模型C组于免疫注射第3周左右开始出现活动减少,倦怠嗜卧,食欲体重下降等表现,模型B组有14只SD大鼠于免疫注射第4～5周出现上述症状,较C组为轻;模型组肌酶谱中,肌酸激酶(CK)、乳酸脱氢酶(LDH)、谷草转氨酶(AST)与对照组比较明显升高,模型C组较模型B组升高更显著;模型组肌电图时限缩短,波幅降低,多相波增多;磁共振检查模型B组和C组选送标本中各有一例有阳性改变,表现为T1MI等或稍低信号,T2MI及STIR序列为高信号,提示肌肉炎症水肿改变;模型B组有11只,模型C组全部大鼠骨骼肌出现病理改变,表现为横纹肌局灶性分布的肌纤维变性炎细胞浸润,间质小血管壁增厚、扩张,随机选送的心肌标本中有3例有阳性改变,表现与骨骼肌相仿,选送的肺标本中有1例有阳性改变,表现为蛋白渗出,炎症细胞浸润和小血管改变。结论:免疫机制与多发性肌炎发病有关;适当的加大抗原免疫剂量可以获得更为典型的动物模型和更高的制模成功率;EAM模型的各种临床特征与人类多发性肌炎相似;本研究采用的造模方法可作为研究人类多发性肌炎的一个重要手段,可为阐明其发病机制及治疗提供科学的理论依据。
[Abstract]:Objective: to study the method of making experimental autoimmune myositis animal model. Methods: SD rats were divided into three groups: group A (n = 8), group B (n = 8), group C (n = 16), group B (n = 16) and group C (n = 16). In order to increase the dose group, the guinea pig skeletal muscle homogenate globulin (15 mg / ml 30 mg / ml) and complete Freund's adjuvant (including BCG vaccine) were used to immunize SD rats in each group with different concentrations of multiple doses of normal saline plus the same amount of CFAB. The model of experimental polymyositis was made by adding the muscle homogenate of 15mg/ml and the muscle homogenate of group C of 30mg/ml with the same amount of CFA. The clinical manifestations, electromyography, myozyme spectrum, magnetic resonance imaging and pathological changes of skeletal muscle, myocardium and lung were observed. In group B, 14 SD rats developed the above symptoms at the 4th week after immunization, which was lighter than that in group C. creatine kinase CKT, lactate dehydrogenase (LDH) and glutamic oxaloacetic transaminase (AST) in the muscle zymogram of the model group were significantly higher than those in the control group. The electromyography duration of model group was shortened, the amplitude of wave was decreased, and the polyphase wave was increased, and one of the selected samples of model group B and group C had positive changes in MRI, and the electromyogram of model group C was significantly higher than that of group B, and the electromyogram of model group was shorter than that of group C. T2MI and STIR sequences of T1MI et al or slightly lower signal intensity were high signal, indicating the change of inflammation and edema of muscle, 11 rats in model group B and all rats in group C had pathological changes in skeletal muscle. The results were as follows: focal distribution of rhabdomytophore infiltration of myofibrodenitis cells, thickening and dilatation of interstitial small vascular wall, positive changes in 3 randomly selected myocardial specimens, which were similar to skeletal muscle. Positive changes were found in 1 of the selected lung specimens, including protein exudation, inflammatory cell infiltration and small vascular changes. Conclusion: the immune mechanism is related to the pathogenesis of polymyositis and the clinical characteristics of EAM model can be similar to those of human polymyositis model. The method used in this study can be used as an important means to study human polymyositis and provide a scientific theoretical basis for elucidating the pathogenesis and treatment of polymyositis.
【学位授予单位】：苏州大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R-332

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