颈内动脉粥样硬化性脑梗死患者外周血内皮祖细胞的变化趋势

The trend in the changing of human peripheral blood endothelial progenitor cells after brain infarction due to carotid atherosclerosis

目的观察急性颈内动脉粥样硬化性脑梗死患者外周血内皮祖细胞数目的变化趋势。方法分别于发病24h,以及第4、7、14和 21天时提取30例成年急性脑梗死患者外周血单个核细胞,流式细胞术检测CD34和CD133表达水平,计数内皮祖细胞数目。结果不同处理组患者各观察时间点外周血内皮祖细胞数目比较,差异均有统计学意义(P=0.000)。脑梗死后24 h,脑梗死组和颈动脉硬化组患行外周血大皮祖细胞数目均低于对照组(P=0.000);脑梗死后第7天,外周血内皮祖细胞数目减少至最低水平(P=0.001),至第21天外毒血内皮祖细胞数目接近颈动脉硬化组水平(P=0.901),但仍低于正常值范围(P=0.000)。内皮祖细胞数目的变化与血小板计数之间不具有相关性(R^2=0.852,P=0.895)。结论颈内动脉系统粥样硬化所致脑梗死患者外周血内皮祖细胞数目低于正常值范围,且于急性期可能存在骨髓动员抑制,同时需要消耗大量内皮祖细胞以进行损伤内皮的修复,使得患者在急性期出现短暂性内皮祖细胞数目减少。

Objective To investigate the trend in the changing of peripheral blood endothelial progenitor cells （EPCs） in patients with acute brain infarction due to atherosclerosis of internal carotid artery. Methods Peripheral blood samples of 30 adults were collected on the first 24 h, and 4, 7, 14 and 21 d after acute brain infarction. Mononuclear ceils were collected. The expressions of CD34 and CD133 were detected by flow cytometry, and the number of EPCs was counted. Results There was significant difference in the number of peripheral blood EPCs among 3 groups at different time points （P = 0.000, for all）. The number of peripheral blood EPCs was significantly lower in brain infarction group and carotid atheroselerosis group at 24 h than that in normal control group （P = 0.000, for all）. The number of peripheral blood EPCs reduced to the lowest level at 7 d in brain infarction group （P = 0.001） and nearly approached to the level of that in carotid atherosclerosis group at 21 d （P = 0.901）, but was still lower than normal range （P = 0.000）. There was no relationship between the number changes of EPCs with platelet count （R2= 0.852, P = 0.895） in the follow-up period. Conclusion Peripheral blood EPCs in patients with brain infarction due to carotid atheroselerosis is lower than normal level. At the acute stage of brain infarction, the bone marrow can be depressed, and amount of EPCs is consumed for repairing the injuried endothelium. Therefore, transient decrease of EPCs is observed at acute stage of brain infarction.