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.
Eon A Kim  1 ,  Ji Ae Kim ,  Mi Hye Park ,  Sung Chul Jung ,  Suk Hyo Suh ,  Myung-Geol Pang ,  Young Ju Kim
Affiliations
  • 1. Department of Obstetrics and Gynecology, Ewha Womans University, Seoul 158-051, Korea.
PMID: 19089771 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.

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