Linked Life Data

19226207

Source:http://linkedlifedata.com/resource/pubmed/id/19226207

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pubmed-article:19226207pubmed:abstractTextLysophosphatidylcholine (LPC) is a lysolipid, acting as a potent cellular mediator of various biological processes. The purpose of this study was to define the role of LPC as a possible causative factor of disrupted redox balance in aged aorta from rats. In this study, we found elevated serum LPC levels in 24-month-old rats that were correlated with the age-related increase in cytosolic phospholipase A(2) (PLA(2)) activity. We also found that aortas from old rats showed increased 5-lipoxygenase (5-LO) activity. With the LPC-treated endothelial cells (YPEN-1 cells), we observed a rapid generation of reactive species, leading to enhanced oxidative stress. Our further investigations using specific 5-LO inhibitors led to the identification of a 5-LO pathway as the reactive species production source in the LPC-treated cells. Additional validation of this 5-LO pathway was made by the detection of increased leukotriene B4 generation in the LPC-treated cells. These in vitro data supported findings of increased expression and activation of aortic 5-LO in old rats by LPC. Together, our data strongly suggested that LPC caused the enhancement of oxidative stress in aged aorta through reactive species generation by an activated 5-LO pathway. LPC may well be an important contributor to age-related oxidative stress in aging aorta.lld:pubmed
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pubmed-article:19226207pubmed:articleTitleLysophosphatidylcholine enhances oxidative stress via the 5-lipoxygenase pathway in rat aorta during aging.lld:pubmed
pubmed-article:19226207pubmed:affiliationCollege of Pharmacy, Aging Tissue Bank, Busan, South Korea.lld:pubmed
pubmed-article:19226207pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19226207pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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