[Aspirin inhibits proliferation and expression of p44/42 MAPK phosphorylation in vascular endothelial cells]

Di Yi Jun Yi Da Xue Xue Bao. 2004 Sep;24(9):1013-5.
[Article in Chinese]

Abstract

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.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aspirin / pharmacology*
  • Cell Proliferation / drug effects*
  • Cells, Cultured
  • Depression, Chemical
  • Endothelial Cells / cytology*
  • Endothelial Cells / metabolism
  • Humans
  • Mitogen-Activated Protein Kinase 1 / biosynthesis*
  • Mitogen-Activated Protein Kinase 1 / genetics
  • Mitogen-Activated Protein Kinase 3 / biosynthesis*
  • Mitogen-Activated Protein Kinase 3 / genetics
  • Phosphorylation / drug effects

Substances

  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3
  • Aspirin