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目的 探索在没有病毒感染的情况下 ,自身免疫机制在心肌炎和心肌病发病中的作用。方法 (1)猪心肌肌球蛋白致BALB/C鼠自身免疫性心肌疾病模型的复制 :实验组 (n =32 )于实验的第 0 ,7和 30天 3次注射肌球蛋白 ,对照组 (n =2 0 )与实验组同样的时间注射弗氏完全佐剂 ,于初次免疫后的第 15 ,2 1和 12 0天分别留取血清和心肌标本。 (2 )病毒性心肌炎模型的复制 :病毒接种组 (n =2 2 )给予 10 3 TCID50 / 0 1mlCVB3 溶液腹腔注射 ,对照组 (n =10 )给予Vero细胞冻融液 0 1ml腹腔注射 ,接种时间及采样时间同肌球蛋白免疫组。 (3)抗体检测 :ELISA法检测小鼠血清抗肌球蛋白抗体。结果 病理结果显示 ,肌球蛋白致心肌炎小鼠急性期 (15和 2 1d)以心肌纤维变性坏死和淋巴细胞浸润较明显 ,间质病变较轻 ,内膜和心瓣膜无明显改变 ;慢性期 (12 0d)仅见心肌纤维化 ,急慢性期均可检测到高滴度的抗肌球蛋白抗体 (P <0 0 0 1) ,对照组为正常心肌 ,抗体滴度低。病毒接种组慢性期亦显示成纤维细胞增生。结论 心肌肌球蛋白可以作为自身抗原刺激机体产生自身免疫反应 ,在没有病毒感染的情况下 ,单一的自身免疫机制即可导致心肌炎向心肌病的转化。
Objective To explore the role of autoimmunity in the pathogenesis of myocarditis and cardiomyopathy without virus infection. METHODS: (1) Replication of porcine cardiomyocyte myosin-induced autoimmune cardiomyopathy in BALB / c mice: In the experimental group (n = 32), myosin was injected three times on days 0, 7 and 30 of the experiment, n = 20) were injected Freund’s complete adjuvant at the same time as the experimental group. Serum and myocardial samples were collected on the 15th, 21st and 12th day after the initial immunization. (2) Replication of viral myocarditis model: 10 3 TCID50 / 0 1 ml CVB3 solution was intraperitoneally injected in the virus inoculation group (n = 2 2), and 0.1 ml Vero freeze-thaw solution was injected intraperitoneally in the control group (n = 10) And the same sampling time with myosin immunization group. (3) Antibody detection: The serum anti-myosin antibody was detected by ELISA. Results The pathological results showed that in the acute phase (15 and 21 days) myosin-induced myocarditis, myocardial fibrosis, necrosis and lymphocyte infiltration were obvious, interstitial lesions were mild, and there was no significant change in the intima and valvular heart. In the chronic phase 12d) only showed myocardial fibrosis, high titer anti-myosin antibody could be detected in both acute and chronic phase (P <0.01), and the control group was normal myocardium with low antibody titer. Chronic viral infection also showed fibroblast proliferation. Conclusion Myocardial myosin can stimulate the body as an autoantigen to produce autoimmune reaction. In the absence of virus infection, a single autoimmune mechanism can lead to the conversion of myocarditis to cardiomyopathy.