商陆皂苷甲作用于子宫内膜异位症大鼠腹腔巨噬细胞蛋白质组的差异分析
Differential proteomics analysis of peritoneal macrophages in endometriosis rat treated by Esculentoside A
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摘要: 目的: 研究商陆皂苷甲作用于子宫内膜异位症大鼠腹腔巨噬细胞蛋白质组的差异,鉴定差异表达的蛋白质。 方法: 采用自体移植法建立子宫内膜异位症大鼠模型。造模成功后取腹腔巨噬细胞,商陆皂苷甲作用24 h后,采用双向凝胶电泳技术分离巨噬细胞总蛋白,并获得药物组、模型组和空白对照组蛋白质组图谱,PDQuest软件分析确认三组细胞的差异蛋白质,最后运用串联飞行时间质谱(MALDI-TOF-TOF MS)鉴定差异蛋白点。 结果: M2型丙酮酸激酶、磷酸酰肌醇转移蛋白和热休克蛋白8在子宫内膜异位症大鼠腹腔巨噬细胞中高表达,而磷酸甘油醛脱氢酶表达减少。商陆皂苷甲能抑制造模引起的M2型丙酮酸激酶等四种蛋白的表达变化。 结论: 利用蛋白质组学技术,研究商陆皂苷甲作用于子宫内膜异位症大鼠腹腔巨噬细胞后蛋白表达差异,为探索子宫内膜异位症的发病机制和商陆皂苷甲的作用机制提供新的线索和依据。Abstract: Objective To evaluate the differential proteomics of the peritoneal macrophages in experimental endometriosis rats treated by EsA. Methods Experimental endometriosis was induced by auto-transplantation of endometrium.Two-dimensional polyacrylamide gel electrophoresis(2D-PAGE) combined with MALDI-TOF/TOF identification were used to investigate the effects of EsA on the proteome of macrophages of experimental endometriosis rats. Results Compared with normal controls,pyruvate kinase3(PKM2).phosphatidylinositol transfer protein(PITPN),and heat shock protein 8(HSP8) had higher expression in peritoneal macrophages of experimental endometriosis,but glyceraldehyde phosphate dehydrogenase(GAPDH) expressed lower.However,these aberrant expression could be inhibited by EsA. Conclusion It was revealed a potential mechanism of the pathogenesis of endometriosis,which gave a new sight to understand the anti-inflammatory effects of EsA and its underlying immunoregulation mechanisms.
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