【摘要】 目的 探讨血管紧张素Ⅱ(AngⅡ)对内皮祖细胞(EPCs)增殖、迁移、黏附功能的影响及MAPK信号通路在其中的作用。方法 取健康成人外周血分离、培养出EPCs并鉴定。以不同浓度AngⅡ(0.1、1、10、100μmol/L)干预,得出最佳浓度用于后续干预实验。分组:对照组、AngⅡ组、JNK抑制剂SP600125+AngⅡ组、ERK1/2抑制剂A6355+AngⅡ组和p38抑制剂PD169318+AngⅡ组。检测各组EPCs的增殖、迁移、黏附能力。结果 AngⅡ对EPCs增值能力无显著影响;AngⅡ可促进EPCs的迁移、黏附功能,在1μmol/L时达到最大效果。AngⅡ对EPCs迁移功能的促进作用能被JNK抑制剂SP600125(P<0.01)、ERK1/2抑制剂A6355(P<0.01)和p38抑制剂PD169318(P<0.05)抑制。其中,ERK1/2抑制剂A6355的抑制作用最显著。AngⅡ对EPCs黏附功能的促进作用可被JNK抑制剂SP600125(P<0.05)、ERK1/2抑制剂A6355(P<0.01)和p38抑制剂PD169318(P<0.05)抑制。结论 AngⅡ可能通过激活MAPK信号通路促进EPCs的迁移、黏附功能。更多还原

【Abstract】 Objective To analyze the effects of angiotensin Ⅱ(Ang Ⅱ) on the proliferation,migration and adhesion of endothelial progenitor cells(EPCs) and the role of MAPK pathway in this process.Methods EPCs were cultured in serum- free EBM- 2 medium for 24 h before incubation with various concentrations of Ang Ⅱ(0.1,1,10,100 μmol/L) for 48 h.EPCs proliferation,migration and adhesion capacities were measured.Choose the best concentrations of Ang Ⅱ.The adherent cells were collected and divided into five groups randomly:control group,Ang Ⅱ group,SP600125 +Ang Ⅱ,A6355 + Ang Ⅱ and PD169318 + Ang Ⅱ group.EPCs proliferation and migration and adhesion were assayed by MTT assay and modified Boyden chamber assay and cell counting respectively.Results Ang Ⅱ significantly increased the migration and adhesive ability of EPCs in a dose- dependent manner,maximum at 1 μmol/L(P < 0.05),but has no effect on proliferative ability.The influence of Ang Ⅱ on EPC migration capacities can be abolished by SP600125(59.3 ± 9.4 vs 113.6 ± 11.2,P < 0.01),A6355(52.1 ±10.4 vs 113.6 ± 11.2,P <0.01)and PD169318(64.6 ± 10.7 vs 113.6 ± 11.2,P<0.05).Similarly,the adhesive capacities can be inhibited by SP600125(41.3 ± 10.2 vs 67.8 ±10.3,P<0.05),A6355(39.6±12.4 vs 67.8 ±10.3,P <0.01)and PD169318(42.1 ±11.6 vs 67.8 ±10.3,P < 0.05).Conclusion Ang Ⅱ improves EPC migration and adhesion capacities through activating MAPK pathway.更多还原