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阿尔茨海默病外周血内皮祖细胞数量及功能的研究 被引量:3

Study of quantity and function of endothelial progenitor cells in peripheral blood of patients with Alzheimer’s disease
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摘要 目的观察内皮祖细胞(EPC)在阿尔茨海默病(AD)外周血中的数量及功能,探讨AD潜在的血管机制。方法选择58例AD患者分为轻度痴呆组19例、中度痴呆组21例和重度痴呆组18例,并以18名无痴呆者作为对照组,采集外周血,分离及培养EPC,采用荧光标记方法评估体外培养EPC数量,同时检测EPC的迁移和黏附功能,分别进行组间EPC数量、迁移和黏附功能的对比。结果4组外周血EPC数量比较差异无统计学意义(P>0.05)。中度痴呆组和重度痴呆组的外周血EPC的迁移和黏附功能均低于轻度痴呆组和无痴呆组(P均<0.05)。结论AD患者的EPC功能下降,导致内皮细胞修复功能降低,这可能与AD的发生发展有关。 Objective To observe the quantity and function of endothelial progenitor cells(EPCs) in the peripheral blood of patients with Alzheimer’s disease,and to explore the potential vascular mechanism of Alzheimer’s disease.Methods Fifty-eight patients with Alzheimer’s disease were divided into the mild(n = 19),moderate(n = 21) and severe groups(n = 18),and 18 normal control were assigned into the control group.The EPCs were isolated from the peripheral blood and cultured in vitro.The quantity of EPCs was evaluated by AC-LDL/lectin fluorescent labeling method,and the migration and adhesion ability of EPCs were detected.The number,migration and adhesion function of EPCs among four groups were statistically compared.Results The number of circulating EPCs did not significantly differ among four groups(all P > 0.05).The migration and adhesion function of circulating EPCs in the moderate and severe groups were significantly lower than those in the mild and control groups(all P < 0.05).Conclusions Patients with Alzheimer’s disease present with decreased EPCs function.The decline in repair function of endothelial cells caused by the vascular mechanism is probably involved in the incidence and development of Alzheimer’s disease.
作者 李海员 徐雪 刘敏 韦伶郁 古钎林 宋汉聪 陈秋蕾 徐嘉 Li Haiyuan;Xu Xue;Liu Min;Wei Lingyu;Gu Xianlin;Song Hancong;Chen Qiulei;Xu Jia(Care Center for the Elderly with Dementia,Home for the Aged Guangzhou,Guangzhou 510550,China)
出处 《新医学》 2020年第8期590-594,共5页 Journal of New Medicine
基金 国家自然科学基金(81801948)。
关键词 阿尔茨海默病 内皮祖细胞 血管机制 Alzheimer’s disease Endothelial progenitor cell Vascular mechanism
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