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目的:研究血管紧张素Ⅱ(AngⅡ)对白血病HL-60骨桥蛋白表达的影响及机制。方法:体外培养HL-60细胞株,予Ang II(终浓度10-9、10-8、10-7、10-6 mol/L)刺激24 h或予AngⅡ(终浓度10-7 mol/L)刺激12h、24 h、48 h;先经PI3K/AKT抑制剂LY294002(40 umol/L)预处理1 h,再予10-7 mol/L Ang II刺激24 h,收集细胞,采用western-blot法检测OPN表达情况。结果:AngⅡ促进HL-60细胞表达OPN,在一定浓度及时间内,其表达量随着AngⅡ浓度和时间的增加而增加,呈剂量和时间依赖性关系;经LY294002预处理再予AngⅡ刺激的HL-60细胞,与对照组比较,OPN表达明显抑制(P<0.05)。结论 :AngⅡ经PI3K/AKT信号通路诱导OPN的表达。
Objective: To investigate the effect of angiotensin Ⅱ (Ang Ⅱ) on osteopontin expression of leukemia HL-60 and its mechanism. Methods: HL-60 cells were cultured in vitro and stimulated with Ang II (final concentration 10-9,10-8,10-7,10-6 mol / L) for 24 h or treated with AngⅡ (final concentration 10-7 mol / L ) Were pretreated with PI3K / AKT inhibitor LY294002 (40 umol / L) for 1 h and then stimulated with 10-7 mol / L Ang II for 24 h. The cells were harvested by western-blot Method to detect OPN expression. Results AngⅡ promoted the expression of OPN in HL-60 cells in a dose-and time-dependent manner. The expression of OPN increased with the increase of Ang Ⅱ concentration and time in a dose-and time-dependent manner. After treatment with LY294002, -60 cells, compared with the control group, OPN expression was significantly inhibited (P <0.05). Conclusion: The expression of OPN was induced by PI3K / AKT signaling pathway.