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目的建立难治性癫痫大鼠模型,通过对海马线粒体蛋白质组的研究,探讨其发病机制并寻找新的治疗靶点。方法应用固相pH梯度等电聚焦和十二烷基硫酸钠-聚丙烯酰胺凝胶电泳(SDS-PAGE)二维电泳,基质辅助激光解析/电离-飞行时间质谱(MALDI-TOF)技术分析和鉴定耐药/非耐药癫痫大鼠海马线粒体差异蛋白。结果耐药组癫痫大鼠海马线粒体19种蛋白表达异常,5种表达上调的蛋白为3-磷酸甘油醛脱氢酶、磷酸丙糖-1、电压依赖性阴离子通道1、醛糖A和微管蛋白,14种表达下调的蛋白质为顺乌头酸酶、谷氨酸脱氢酶、苹果酸脱氢酶、NADH脱氢酶、ATP合成酶、丙酮酸激酶同工酶类似物、ATP结合盒B亚家族、磷脂酶A2、丝氨酸蛋白酶抑制剂、热休克蛋白、解偶联蛋白、Cofilin1、醛脱氢酶和电压依赖性阴离子通道2。结论难治性癫痫大鼠海马线粒体存在大量差异表达蛋白,可能参与癫痫耐药的发生。
Objective To establish a rat model of intractable epilepsy by exploring the mitochondrial proteome of hippocampus and to explore its pathogenesis and to find new therapeutic targets. METHODS: Solid-phase pH gradient isoelectric focusing and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) two-dimensional electrophoresis were used to analyze and analyze the effects of MALDI-TOF Identification of hippocampal mitochondrial differential proteins in drug-resistant / non-drug resistant epileptic rats. Results The protein expression of mitochondria in the hippocampus of the drug-resistant epilepsy rats was abnormal. The five proteins upregulated were glyceraldehyde-3-phosphate dehydrogenase, triosephosphate-1, voltage-dependent anion channel 1, aldose A and microtubules Protein, and the 14 proteins whose expression was down-regulated were aconitase, glutamate dehydrogenase, malate dehydrogenase, NADH dehydrogenase, ATP synthase, pyruvate kinase isozyme analogs, ATP binding cassette B Subfamily, phospholipase A2, serine protease inhibitors, heat shock proteins, uncoupling proteins, Cofilin1, aldehyde dehydrogenases and voltage-dependent anion channels 2. Conclusion There are a large number of differentially expressed proteins in the hippocampus of refractory epilepsy rats, which may be involved in the development of epilepsy resistance.