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目的用革兰阴性菌细胞壁成分脂多糖(lipopolysaccride,LPS)刺激大脑皮质混合胶质细胞,检测高迁移率族蛋白-1(HMGB-1)的表达情况与转位作用,了解HMGB-1与其他炎性介质相互作用参与神经胶质细胞介导脑部炎症反应的机理。方法体外培养小鼠大脑皮质混合胶质细胞,采用1μg/ml LPS刺激,收集细胞以及培养上清,Westernblotting检测混合胶质细胞HMGB-1的蛋白水平;免疫荧光法检测HMGB-1的转位情况;Griess法检测培养上清中NO的水平。结果 LPS刺激下,大脑皮质混合胶质细胞HMGB-1的蛋白表达水平增加并向胞浆中移位,与正常对照组比较差异有统计学意义(P<0.05);NO与HMGB-1变化趋势一致,水平增加,与正常对照组比较差异有统计学意义(P<0.01)。结论 LPS刺激模拟革兰阴性菌感染,大脑皮质混合胶质细胞产生的HMGB-1与NO协同参与了其介导的脑部炎症反应。
Objective To investigate the expression and translocation of high mobility group box-1 (HMGB-1) stimulated by mixed with glial cells of the gram-negative bacterial cell wall lipopolysaccride (LPS) to understand the relationship between HMGB-1 and other Inflammatory mediators are involved in the mechanism of glial cell-mediated brain inflammatory response. Methods Cultured mouse cerebral cortex mixed glial cells in vitro, stimulated with 1μg / ml LPS, collected cells and culture supernatants, Western blotting assay HMGB-1 protein levels; immunofluorescence assay HMGB-1 translocation The level of NO in culture supernatant was detected by Griess method. Results The protein expression of HMGB-1 in the mixed cortical neurons of the cerebral cortex increased and shifted to the cytoplasm under LPS stimulation compared with the normal control group (P <0.05). The change trend of NO and HMGB-1 Consistent with the level increased, compared with the normal control group, the difference was statistically significant (P <0.01). Conclusions LPS stimulates the infection of Gram-negative bacteria. HMGB-1 produced by mixed cortical neurons in the cerebral cortex participates in the mediation of brain inflammatory response mediated by LPS.