摘要
目的观察阿司匹林对体外培养的血管内皮细胞的增殖和磷酸化p44/42丝裂素活化蛋白激酶(MAPK)表达的影响。方法体外培养血管内皮细胞株ECV304,应用1、2、5、10 mmol/L的阿司匹林分别作用并设立对照进行比较,采用MTS/PES法确定ECV304细胞的增殖状态。利用p44/42磷酸化抗MAPK抗体的蛋白免疫印迹法测定磷酸化p44/42 MAPK蛋白表达。结果各组的细胞增殖率分别为对照组1.533±0.286,阿司匹林1 mmol/L组1.253±0.225,2 mmol/L组0.953±0.149,5 mmol/L组0.708±0.125,10 mmol/L组0.459±0.107。统计分析显示低至1 mmol/L的阿司匹林仍能明显抑制ECV304细胞的增殖(P<0.05),并呈现剂量依赖性。阿司匹林对ECV304细胞的磷酸化p44/p42 MAPK表达有显著的抑制作用(P<0.05)。结论阿司匹林对体外培养的血管内皮细胞的增殖和内皮细胞中磷酸化p44/42 MAPK的表达均有明显的抑制作用。
Objective To observe the effects of aspirin on vascular endothelial cell proliferation in vitro and on the activity of p44/p42 mitogen-activated protein kinase (MAPK) phosphorylation. Methods ECV 304 cells cultured in vitro were treated with aspirin (1, 2, 5, and 10 mmol/L, respectively) and observed for their proliferation in comparison with the control group. The ratio of cell proliferation was determined by non-radioactive MTS/PES assay. The expression of phosphorylated p44/42 MAPK protein was evaluated by the immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Results The proliferation rate of the endothelial cell was 1.533±0.286 in the control group, and 0.459±0.107, 0.708±0.125, 0.953±0.149 and 1.253±0.225 in aspirin-treated groups corresponding to aspirin concentrations of 10, 5, 2 and 1 mmol/L, respectively. It was shown that aspirin significantly inhibited the vascular endothelial cell proliferation at the concentration above 1 mmol/L (P<0.05), in a dose-dependent manner as compared with the control group (P<0.05). The expression of phosphorylated p44/42 MAPK protein was significantly inhibited by aspirin. Conclusions Aspirin decreases vascular endothelial cell proliferation, and arrest of endothelial cell proliferation may be an important mechanism by which aspirin produces protective effect against acute coronary disease.
出处
《第一军医大学学报》
CSCD
北大核心
2004年第9期1013-1015,共3页
Journal of First Military Medical University
基金
广州市科委科技攻关项目(JB00000448165)~~
关键词
阿司匹林
内皮细胞
细胞增殖
丝裂素活化蛋白激酶
aspirin
endothelial cells
cell proliferation
mitogen-activated protein kinase
