| 摘要: |
| 目的观察黄芪甲苷对3，4苯并芘（BaP）介导内皮祖细胞（EPCs）损伤的保护作用并探讨其机制。方法采用密度梯度离心法收集人脐血单个核细胞，贴壁培养法培养EPCs，消化收集第4代细胞，随机分为5组，正常对照组：不作任何处理；Bap组：予BaP，浓度为20μmol/L；3种浓度黄芪甲苷各组（先加入浓度分别为2、10、50μg/ml的黄芪甲苷，2h后再加入浓度为20μmol/L的Bap）。分别采用细胞计数试剂盒（CCK-8）检测细胞增殖能力，黏附能力测定实验检测细胞黏附能力，transwell小室检测细胞迁移能力。取各组细胞培养上清液检测其超氧化物歧化酶（SOD）及丙二醛（MDA）含量，免疫荧光染色检测各组细胞活性氧（ROS）的表达。结果与正常对照组相比，BaP组细胞的增殖、黏附以及迁移能力均明显降低（均P＜0.01），黄芪甲苷预保护可呈浓度依赖性地提高EPCs增殖、黏附及迁移能力（均P＜0.05）；BaP组培养上清液中MDA含量与正常对照组相比明显升高（P＜0.01），SOD含量明显下降（P＜0.01），ROS表达明显上升（P＜0.01），不同浓度的黄芪甲苷可降低培养上清液中MDA含量（P＜0.05），提高SOD含量（P＜0.05），并且呈浓度依赖性地降低细胞ROS表达（P＜0.01）。结论黄芪甲苷对BaP介导的EPCs损伤具有保护作用，其机制可能与抑制氧化应激有关。 |
| 关键词: 3，4 苯并芘 内皮祖细胞 黄芪甲苷 氧化应激 |
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| Protective effect of astragaloside IV on benzo [a] pyrene-mediated endothelial progenitor cell dysfunction and its mechanism |
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Chen Jun,Xia Wujie,Xue Yangjing,Hu Jianjian
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the First Affiliated Hospital of Wenzhou Medical University
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| Abstract: |
| Objective To investigate the protective effect of Astragaloside IV (As IV) on benzo [a] pyrene (BaP)-mediated endothelial progenitor cell (EPC) dysfunction and to explore the underlying mechanism. Methods Human umbilical cord blood mononuclear cells were seeded in adherent culture to obtain EPCs. The EPCs were divided into 3 groups: control group, BaP group, and As IV group. BaP and Ac IV groups were treated with 20μmol/L BaP for 24h, and before exposure to BaP the As IV groups were pre-treated with different concentrations of Astragaloside IV (2, 10 and 50μg/ml) for 24h. The proliferation, adhesion and migration of EPCs were evaluated by CCK-8 method, adhesion assay and Transwell assay, respectively. The superoxide dismutase (SOD) and malondialdehyde (MDA) levels in culture supernatants were measured, and the expression of ROS was detected by immunofluorescence staining. Results Compared to the control group, BaP-treated EPCs showed a decline in proliferation, adhesion and migration (P ＜0.01); while As IV treatment significantly attenuated BaP-induced decline of cell proliferation, adhesion and migration (P＜0.05) in EPCs. Furthermore, BaP-treated EPCs presented an increasing expression of
ROS and MDA, but a decline of SOD secretion (P＜0.01); while various concentrations of Astragaloside IV reduced the production of MDA (P＜0.05) and ROS (P＜0.01), and increased the SOD activity (P＜0.05) of EPCs in a concentration-dependent manner. Conclusion Astragaloside IV is able to prevent BaP-mediated EPCs dysfunction, probably by inhibiting oxidative stress. |
| Key words: Benzo[a]pyrene (Bap) Endothelial progenitor cells (EPCs) Astragaloside IV Oxidative stress |
