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糖基化终产物对小胶质细胞分泌IL-1β和TNF-α的影响
被引:10
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刘雪平
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机构: 山东大学附属省立医院老年神经科

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[1] 山东大学附属省立医院老年神经科
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关键词:
阿尔茨海默病;
糖基化终产物,高级;
白细胞介素1;
肿瘤坏死因子;
小神经胶质细胞;
大鼠,Wistar;
D O I:
暂无
中图分类号:
R749.16 [];
学科分类号:
摘要:
目的研究糖基化终产物(AGEs-BSA)对原代培养的小胶质细胞分泌白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的影响,在细胞水平探讨AGEs-BSA在阿尔茨海默病(AD)发生中的作用及其可能机制。方法体外培养小胶质细胞,用AGEs-BSA干预,用免疫细胞化学方法,进行鉴定并观察其形态变化;用AGEs-BSA300μg/mL激活和抗RAGE中和抗体阻断的方法对原代培养的小胶质细胞进行处理,用酶联免疫吸附法(ELISA)检测细胞上清液中IL-1β和TNF-α的水平。结果 AGEs-BSA干预后小胶质细胞胞体变大,形态不规则,呈"阿米巴样",细胞上清液中IL-1β、TNF-α浓度均明显升高(P<0.001),抗RAGE中和抗体+AGEs-BSA组细胞上清液IL-1β、TNF-α浓度较AGEs-BSA组呈下降趋势(P<0.01),但仍高于正常对照组(P<0.01)。结论 AGEs-BSA可激活小胶质细胞,诱导其释放IL-1β和TNF-α,并呈时间依赖性。提示糖基化终产物能直接或通过作用其受体激活小胶质细胞介导的免疫炎性反应。
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页码:34 / 38
页数:5
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