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目的:采用蛋白质组学技术研究氟桂利嗪对脑缺血再灌注大鼠脑组织差异蛋白进行,进一步揭示氟桂利嗪的脑保护作用及抗损伤修复机制。方法:建立脑缺血再灌注大鼠动物模型,分别提取蛋白质,2-DE电泳分离,应用相关软件比较分析,找出差异蛋白,酶切消化后进行肽指纹图谱分析,数据检索,初步鉴定差异蛋白质。结果:局灶性脑缺血模型组与氟桂利嗪干预组的比较蛋白质组学研究。与模型组比较,从氟桂利嗪干预组找到了25个差异表达蛋白斑点,其中10个低表达,15个高表达,鉴定其中6个蛋白质,发现激肽原-1前体、谷氨酸受体前体等与脑缺血相关的蛋白质。结论:氟桂利嗪对脑缺血再灌注的保护作用是多个蛋白共同参与的结果。
OBJECTIVE: To study the effect of flunarizine on differentially expressed proteins in brain tissue of rats with cerebral ischemia-reperfusion injury by using proteomics technology, and to further reveal the neuroprotective effect of flunarizine and the mechanism of anti-injury repair. Methods: Animal models of cerebral ischemia / reperfusion were established. Proteins were isolated and separated by 2-DE. The relative proteins were compared and analyzed to identify the differentially expressed proteins. Peptide fingerprinting, data search and preliminary identification of differences protein. Results: A comparative proteomics study between focal cerebral ischemia model group and flunarizine intervention group. Compared with the model group, 25 differentially expressed protein spots were found in the flunarizine intervention group, of which 10 were low expression and 15 were high expression, of which 6 proteins were identified and found that kininogen-1 precursor, glutamic acid Receptor precursor and other cerebral ischemia-related proteins. Conclusion: The protective effect of flunarizine on cerebral ischemia-reperfusion is the result of multiple proteins participating together.