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目的:探讨CD4+CD25+调节性T细胞(CD4+CD25+ regulatory T cells,Tregs)对氧化型低密度脂蛋白(ox-LDL)致人外周血内皮祖细胞(EPCs)损伤的保护机制。方法:密度梯度离心法分离单个核细胞,培养7d后收获EPCs;磁性细胞分离器(MACS)分离获得Tregs。流式细胞仪鉴定EPCs及Tregs纯度。实验随机分为对照组,ox-LDL组(50mg/L)及ox-LDL+Tregs组,干预24h后,取各组细胞上清液行超氧化物歧化酶(SOD)、丙二醛(MDA)含量检测。收获各组细胞行凋亡相关基因Bcl-2及一氧化氮(NO)的检测。结果:与对照组比较,ox-LDL作用于EPCs后,其SOD,Bcl-2及NO含量显著下降、MDA含量显著升高;Tregs干预24h后,显著改善了EPCs的功能,各组SOD,Bcl-2及NO含量显著升高,MDA含量显著减少。结论:Tregs对ox-LDL致EPCs损伤有显著保护作用,其机制可能与其抗氧化损伤、抗凋亡及促进EPCs的动员与分化有关。
Objective: To investigate the protective mechanism of CD4 + CD25 + regulatory T cells (Tregs) on the injury of human peripheral blood endothelial progenitor cells (EPCs) induced by ox-LDL. Methods: Mononuclear cells were isolated by density gradient centrifugation and cultured for 7 days. Tregs were isolated by magnetic cell separator (MACS). Flow cytometry was used to identify the purity of EPCs and Tregs. The experiment was randomly divided into control group, ox-LDL group (50mg / L) and ox-LDL + Tregs group. After 24h intervention, superoxide dismutase (SOD) ) Content test. The apoptosis-related genes Bcl-2 and nitric oxide (NO) were harvested in each group. Results: Compared with the control group, the levels of SOD, Bcl-2 and NO were significantly decreased and the content of MDA was significantly increased after treated with ox-LDL for 24 h. The intervention of Tregs significantly improved the function of EPCs, -2 and NO content increased significantly, MDA content decreased significantly. CONCLUSION: Tregs have a significant protective effect on EPCs induced by ox-LDL, and its mechanism may be related to its anti-oxidative damage, anti-apoptosis and promotion of EPCs mobilization and differentiation.