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【目的】研究脾胃虚损型重症肌无力(myasthenia gravis,MG)患者与正常人骨骼肌蛋白的差异性表达情况,以探讨MG的发病机制。【方法】采用双向电泳技术对脾胃虚损型MG患者与正常人的骨骼肌蛋白进行分离,采用Image Master 2D platinum 5.0软件对所得的图像进行分析,寻找差异性蛋白。对比值≥1.5的差异蛋白点运用基质辅助激光解吸电离—飞行时间质谱法进行鉴定,在IPI数据库进行搜索,寻找匹配的相关蛋白质。【结果】通过双向电泳技术分析,在实验组脾胃虚损型MG患者与正常对照组骨骼肌中共找到27个表达差异的蛋白质斑点,其中实验组呈低表达,对照组呈高表达的有14个蛋白质点;实验组呈高表达,对照组呈低表达的有13个蛋白质点。对27个表达差异的蛋白质点中选择比值较大的15个蛋白质点进行质谱鉴定,共鉴定出10个蛋白。【结论】MG的发病和(或)病理过程可能是多种机制参与的结果,与骨骼肌收缩有关的肌细胞结构蛋白表达变化、线粒体能量代谢障碍、钙通道以及氧自由基等均可能与此相关,MG与纤维蛋白原及其肽链,MG并发胸腺增生或胸腺瘤与ADP-Ribosylarginine Hydrolase是否存在关系,尚不明确。
【Objective】 To investigate the differential expression of skeletal muscle protein in spleen and stomach patients with myasthenia gravis (MG) and normal subjects to explore the pathogenesis of MG. 【Method】 The skeletal muscle protein of spleen-stomach deficient MG patients and normal individuals were separated by two-dimensional gel electrophoresis. The images were analyzed by Image Master 2D platinum 5.0 software to find differential proteins. Differential protein spots with a value of ≥1.5 were identified using matrix-assisted laser desorption / ionization-time of flight mass spectrometry and searched in the IPI database for matched matching proteins. 【Results】 The results of two-dimensional electrophoresis showed that there were 27 protein spots in skeletal muscle of spleen-stomach-deficient MG patients and normal control group in the experimental group, of which there were 14 low-expression protein spots in the experimental group and 14 high-expression in the control group Protein spots; experimental group was high expression, the control group showed low expression of 13 protein spots. A total of 10 protein spots were identified by mass spectrometry in 15 of the 27 protein spots with different ratios. 【Conclusion】 The onset and / or pathological process of MG may be the result of various mechanisms involved. The structural protein expression of muscle cells related to skeletal muscle contraction, the energy metabolism of mitochondria, calcium channels and oxygen free radicals may all be related to Related, MG and fibrinogen and its peptide chain, MG complicated with thymus hyperplasia or thymoma and ADP-Ribosylarginine Hydrolase whether there is a relationship, it is not clear.