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

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.

Keywords:

• Lysophosphatidylcholine
• endothelium
• nitric oxide
• ROS
• antioxidant
• eNOS