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

Authors
Kim, Eon A.Kim, Ji AePark, Mi HyeJung, Sung ChulSuh, Suk HyoPang, Myung-GeolKim, Young Ju
Issue Date
2009
Publisher
TAYLOR & FRANCIS LTD
Keywords
Lysophosphatidylcholine; endothelium; nitric oxide; ROS; antioxidant; eNOS
Citation
JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE, v.22, no.4, pp 325 - 331
Pages
7
Journal Title
JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE
Volume
22
Number
4
Start Page
325
End Page
331
URI
https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/23478
DOI
10.1080/14767050802556075
ISSN
1476-7058
1476-4954
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 NG-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 (p0.05). 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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대학원 (동물생명공학과.)
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