Lysophosphatidylcholine induces endothelial cell injury by nitric oxide production through oxidative stress

J Matern Fetal Neonatal Med. 2009 Apr;22(4):325-31. doi: 10.1080/14767050802556075.

Abstract

Objective: To determine whether lysophosphatidylcholine (LPC) induces endothelial cell injury by altering the production of nitric oxide (NO) and thereby increasing reactive oxygen species (ROS).

Methods: Human umbilical vein endothelial cells (HUVECs) were cultured and exposed to LPC, LPC with N(G)-nitro-l-arginine methyl ester (L-NAME), LPC with antioxidants. LPC-induced cell injury and viability were determined using LDH and Resazurin assays. The Mann-Whitney U test was used for statistical analysis.

Results: LPC induced HUVEC injury in a concentration-dependent manner. LPC induced the overproduction of NO and ROS in HUVECs and LPC-induced HUVEC injury is significantly inhibited by the eNOS inhibitor (L-NAME) and the antioxidants (p < 0.05).

Conclusions: These findings suggest that LPC induces the overproduction of NO, which may increase the oxidative stress on endothelial cells and lead to endothelial cell injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antioxidants / pharmacology
  • Cell Survival / drug effects
  • Cells, Cultured
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Fluoresceins / metabolism
  • Humans
  • Lysophosphatidylcholines / pharmacology*
  • NG-Nitroarginine Methyl Ester / pharmacology
  • Nitrates / metabolism
  • Nitric Oxide / biosynthesis*
  • Nitrites / metabolism
  • Oxidative Stress*
  • Reactive Oxygen Species / metabolism*
  • Umbilical Veins / cytology

Substances

  • Antioxidants
  • Fluoresceins
  • Lysophosphatidylcholines
  • Nitrates
  • Nitrites
  • Reactive Oxygen Species
  • diacetyldichlorofluorescein
  • Nitric Oxide
  • NG-Nitroarginine Methyl Ester