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目的观察黄芪甲苷对氧化低密度脂蛋白(oxidative low density lipoprotein,ox-LDL)介导的内皮祖细胞(endothelial progenitor cells,EPCs)炎症损伤的保护作用并探讨其可能机制。方法密度梯度离心法获取外周血单个核细胞,贴壁法培养EPCs。培养7 d后,收集贴壁细胞并随机分为对照组、ox-LDL组(100μg·mL 1)及黄芪干预组(ox-LDL 100μg·mL 1加黄芪甲苷,浓度分为2,10和50μg·mL 1),干预24 h后分别采用Matrigel体外成血管试验、Transwell小室法、黏附能力测定实验及细胞计数试剂盒(Cell Counting Kit-8,CCK-8)观察ox-LDL对EPCs成血管能力、迁移能力、黏附能力及增殖能力的影响,并取各组细胞培养上清液行白细胞介素-6(IL-6)和肿瘤坏死因子α(TNF-α)含量检测。结果 ox-LDL损伤后,外周血EPCs的成血管能力、迁移能力、黏附能力及增殖能力显著受损,伴随细胞上清液IL-6及TNF-α水平显著升高;黄芪甲苷干预24 h后,显著改善了EPCs的成血管、迁移、黏附及增殖能力,且黄芪甲苷各组IL-6及TNF-α水平显著降低。结论黄芪甲苷对ox-LDL损伤后EPCs的细胞生物学功能有显著保护作用,其机制可能与抗炎症损伤有关。
Objective To observe the protective effect of astragaloside against oxidative low density lipoprotein (ox-LDL) -mediated inflammatory injury of endothelial progenitor cells (EPCs) and to explore its possible mechanism. Methods Peripheral blood mononuclear cells were obtained by density gradient centrifugation and EPCs were cultured by adherent method. After cultured for 7 days, adherent cells were collected and randomly divided into control group, ox-LDL group (100μg · mL 1) and Astragalus intervention group (ox-LDL 100μg · mL 1 plus Astragaloside Ⅳ, 50μg · mL 1). After intervention for 24 h, Matrigel in vitro angiogenesis assay, Transwell chamber assay, adhesion assay and cell counting kit (Cell Counting Kit-8, CCK-8) Ability, migration ability, adhesion ability and proliferation ability of the supernatant of each group were measured. The levels of IL-6 and TNF-α in each group were measured. Results After ox-LDL injury, the ability of blood vessel formation, migration, adhesion and proliferation of peripheral blood EPCs were significantly impaired accompanied by a significant increase of the levels of IL-6 and TNF-α in the supernatant of the cells. Astragaloside IV intervention for 24 h , Significantly improved the angiogenesis, migration, adhesion and proliferation of EPCs, and significantly decreased the levels of IL-6 and TNF-α in each group. Conclusion Astragaloside has a significant protective effect on the biological function of EPCs after ox-LDL injury, and its mechanism may be related to the anti-inflammatory injury.