摘要
目的探讨阿尔茨海默病(AD)发病的免疫炎性机制.方法体外培养小胶质细胞,免疫细胞化学方法进行小胶质细胞鉴定;用0.1~20 μg/ml聚集状态的β-淀粉样蛋白(Aβ)激活小胶质细胞,观察其形态变化,ELISA法检测培养基中白细胞介素1β(IL-1β)的浓度.结果 0.1 μg/ml Aβ1~42实验组,小胶质细胞形态无明显改变,培养基中IL-1β浓度无明显升高;1 μg/ml和20 μg/ml Aβ1~42实验组,小胶质细胞胞体变大,形态由分枝状转变成'阿米巴样',培养基中IL-1β浓度升高;与对照组比较差异均有显著性意义(均P<0.05).结论 Aβ可激活小胶质细胞,诱导其释放IL-1β,并呈剂量依赖性,提示小胶质细胞介导的免疫炎性机制在AD发病中起着重要的作用.
Objective To study the role of inflammatory response in Alzheimer disease (AD). Methods Cultured microglial cells were treated with or without Aβ1-12 in different concentrations, then the cell morphology and IL-1β secretion were oberserved by microscopy and ELISA seperately. Results In the experimental group of 0.1 μg/ml Aβ1-12 , the shape of microglial cells and the level of IL-1β in culture medium had no change compared with the control group. In the 1 μg/ml and 20μg/ ml Aβ1-12 groups, the levels of IL-1β were significant higher than in the control group; the cell body became bigger and the shape changed from “branch” to “Ameba”. Conclusion Aβ could activate microglia and induce the dose-dependent release of IL-1β, which indicated the importance of the inflammatory mechanism mediated by microglia in AD.
出处
《华中科技大学学报(医学版)》
CAS
CSCD
北大核心
2005年第5期568-571,共4页
Acta Medicinae Universitatis Scientiae et Technologiae Huazhong
基金
湖北省自然科学基金资助项目(No.2001ABB140)