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目的:探讨喹诺酮类抗生素对重症肌无力(MG)治疗的安全性及其引起肌无力加重反应的可能机制。 方法:以丁氏双鳍电鳐电器官的乙酰胆碱受体(AchR)提取蛋白主动免疫C57BL/6小鼠建立实验性自身免疫性 MG(EAMG)模型,随机将EAMG小鼠分为未处理组(A组),生理盐水组(B组)和喹诺酮类抗生素组(C组),分别 于末次免疫后第7天和注射抗生素后第14天进行低频重复电刺激(RNS)检查和血清中AchR抗体(AchRab)水平 的检测。结果:成功复制EAMG小鼠44只;注射抗生素后第14天RNS衰减率和AchRab滴度,C组明显高于A 组(P<0.05及P<0.01)。结论:喹诺酮类抗生素加重MG症状的机理可能与药物提高血清AchRab水平,增加肌 无力评分和肌肉电活动的衰减,从而加重MG神经肌肉接头间传递功能的障碍有关。
Objective: To investigate the safety of quinolone antibiotics in the treatment of myasthenia gravis (MG) and the possible mechanism of its aggravating reaction. Methods: The experimental autoimmune MG (EAMG) model was established by actively immunizing C57BL / 6 mice with acetylcholine receptor (AchR) extracted from Dictyzins trifurcata. EAMG mice were randomly divided into untreated group (Group A), saline group (group B) and quinolone antibiotic group (group C). Low-frequency repetitive electrical stimulation (RNS) and serum AchR antibody were detected on the 7th day after the last immunization and on the 14th day after the injection of antibiotics (AchRab) level of detection. RESULTS: Forty-four EAMG mice were successfully replicated. The RNS decay rate and AchRab titer on the 14th day after antibiotic injection were significantly higher in group C than those in group A (P <0.05 and P <0.01). Conclusion: The mechanism of quinolone antibiotics aggravating the symptoms of MG may be related to increasing the level of serum AchRab, increasing the score of myasthenia gravis and the decay of muscle electrical activity, thus aggravating the disorder of MG neuromuscular junction transfer.