氧化低密度脂蛋白致损人单核细胞白血病细胞株源性巨噬细胞Notch信号的表达

目的 研究氧化型低密度脂蛋白（ox-LDL）致损人单核细胞白血病细胞株（THP1）源巨噬细胞Notch信号的表达,探讨Notch信号各成分对动脉粥样硬化（AS）发病的可能作用。方法 用不同浓度的ox-LDL刺激THP1源巨噬细胞,在不同时间分别应用实时定量聚合酶链式反应及蛋白免疫印迹检测Notch信号通路受体配体的差异表达。结果 与对照组比较,加入ox-LDL后,THP1源巨噬细胞四种受体中Notch1表达明显升高（P〈0. 05）,五种配体中DlL4和Jagged1表达明显升高（P〈0. 05）;Notch1、DlL4和Jagged1升高的作用在ox-LDL浓度为50 mg/ L 6 h点作用最强。结论 ox-LDL致损THP1源巨噬细胞参与AS的发生与Notch1,DlL4和Jagged1高表达有关。

The effect of oxidized low-density lipoprotein on Notch signal expression in macrophages

Objective To explore the expression of Notch signal by oxidized low-density lipoprotein（ox-LDL） in mac- rophages of human monocytic leukemia cell line（ THP1 ） and to search for possible mechanism of atherosclerosis （ AS ）. Methods Human macrophage from THP1 cell line transform by PMA was cultured with different concentration of ox-LDL at different time to induce proinflammatory response. The expression of four receptors and five ligands of Notch mRNA and protein were measured by RT-PCR and Western blot respectively. Results The compared with control group, with the joining of ox-LDL, Notch 1 expression in four receptors of macrophages increased significantly（P〈0.05）, DIL 4 and Jag- ged 1 expression in five ligands increased significantly（P〈0.05 ） ; The expression of Notch 1, DIL 4 and Jagged 1 signifi- cantly increased in ox-LDL concentration of 50 mg/L at 6 h point which was strongest. Conclusion Notchl ,DIIA,Jag- gedl were activated by ox-LDL stimulation and may partially mediate atherogenic effect macrophage functions.