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.
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.
Authors: Nadja S Sieber-Ruckstuhl; Wai Kin Tham; Franziska Baumgartner; Jeremy John Selva; Markus R Wenk; Bo Burla; Felicitas S Boretti Journal: Metabolites Date: 2022-03-30