Objective To investigate the relationship between vitamin D and endothelial progenitor cells in patients with active systemic lupus erythematosus(SLE),and to reveal the intrinsic causes of atherosclerosis in SLE. Methods Thirty consecutive patients(SLEDAI score≥8)were in the active phase of SLE who attended the in-patient clinic of our hospital and 30 age and sex-matched healthy people as controls. Ezyme linked immune sorbent assay(ELISA)was used to detect the levels of 25-Dihydroxyvitamin D[25(OH)D]in peripheral blood. Isolation and culture of endothelial progenitor cells(EPC)by density gradient centrifugation and adherent culture. CD3+/CD4+/VEGFR-2+EPC numbers were determined by flow cytometry. Migration and adhesion of EPCs were observed by transwell migration assay. Statistical analysis was conducted with t-test and Mann-Whitney rank test. Results ①The level of peripheral blood 25(OH)D in patients with active SLE(14.47±10.39)ng/mL was lower than normal controls(24.15±7.98)ng/mL(P<0.05).②In active SLE subgroups，the number of EPC（0.028%±0.017%）were significantly lower than normal controls（0.067%±0.012%）（P ＜0.05）. The migration rate of EPC from active SLE patients（1.7‰ ±0.9‰）were significantly reduced as compared with normal controls（3.1‰±1.6‰）（P ＜0.05）. The adhesion of EPCs from active SLE patients（19±7）were declined as compared with normal controls（34±11）（P ＜0.05）. ③The level of peripheral blood 25（OH）D was positively correlated with the number of EPC in active SLE（P ＜0.05）. The level of peripheral blood 25（OH）D was positively correlated with the migration and adhesion of EPC in active SLE（P ＜0.05）. Conclusion The study demonstrate an association between EPC reduction/dysfunction and vitamin D insufficiency in SLE patients，which results in endothelial dysfunction and atherosclerosis. These findings can provide strong rationale for atherosclerosis therapy in SLE.%目的 研究活动期系统性红斑狼疮患者维生素D水平与内皮祖细胞数量及功能的相关性,揭示系统性红斑狼疮发生动脉粥样硬化的内在原因.材料与方法 收集30例系统性红斑狼疮活动性指数评分大于8分、病情均处于活动期的系统性红斑狼疮患者,30例年龄与性别匹配的健康人作为正常对照组;酶联免疫吸附试验检测外周血25羟基维生素D水平;密度梯度离心和贴壁培养法分离培养内皮祖细胞,流式细胞术检测CD3+/CD4+/VEGFR?2+内皮祖细胞在全血中的比例;通过计数再贴壁和构建侵袭小室检测内皮祖细胞粘附和迁移能力.结果 ①活动期系统性红斑狼疮患者外周血25羟基维生素D(14.47±10.39)ng/mL水平低于健康对照组(24.15±7.98)ng/mL,差异有统计学意义(P<0.05);②体外培养过程中,活动期系统性红斑狼疮患者内皮祖细胞数量(0.028%±0.017%)显著低于正常对照组(0.067%±0.012%);活动期系统性红斑狼疮患者内皮祖细胞迁移率[(1.7‰±0.9‰)vs.(3.1‰±1.6‰)]及粘附能力[(19±7)vs.(34±11)]显著低于正常对照组,差异有统计学意义(P<0.05);③活动期系统性红斑狼疮患者25羟基维生素D水平与内皮祖细胞数量、迁移及粘附功能均呈正相关(P<0.05).结论 系统性红斑狼疮患者维生素D缺乏与内皮祖细胞数量和/或功能异常有关,参与了血管内皮的损伤以及修复障碍,从而增加了动脉粥样硬化发生的风险.
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