title: [Effect of 11, 12-epoxyeicosatrienoic acids on hypoxia/reoxygenation injury in the human umbilical vein endothelial cells].
abstract: OBJECTIVE
  To investigate the effects of 11, 12-epoxyeicosatrienoic acids (11, 12-EET) on the degree of hypoxia/reoxygenation injury in human umbilical vein endothelial cells ( HUVECs), and reveal the possible pathway of EET on protection.
  
  
  METHODS
  Primary cultured HUVECs were randomly divided into control group, hypoxia/reoxygenation group, 11, 12-EET control group, 11, 12- EET hypoxia/reoxygenation group, inhibition of extracellular signal-regulated kinase (ERKI/2) group, and inhibition of nitric oxide synthase (NOS) group. Hypoxia/reoxygenation injury model in HUVECs was established by exposure to hypoxia (2% O2, 5% CO2 and 93% N2) for 3 hours, followed by reoxygenation (95% air and 5% CO2) for 1 hour. The evaluation of the endothelial cells were made by immunohistochemistry. The cell viability was monitored by MTT assay. Colorimetry method was used to assay the lactate dehydrogenase (LDH) , malondialdehyde (MDA) and activity of superoxide dismutase (SOD) in culture medium. Western blot was used to detect the expressions of endothelial nitric oxide synthase (eNOS) and phosphorylated ERK1/2 in HUVECs.
  
  
  RESULTS
  11, 12-EET caused minor injury in normal oxygen incubated HUVECs; however, in hypoxia/reoxygenation HUVECs, it raised the cell viability markedly, decreased the LDH release and MDA content, and increased the activity of SOD and the expressions of eNOS and phosphorylated ERK1/2.
  
  
  CONCLUSIONS
  11, 12-EET may prevent against endothelial cell hypoxia/reoxygenation injury. The mechanism may be related to the increased activity of SOD, elimination of oxygen-derived free radicals, and reduction of eNOS and phosphorylated ERK1/2 lesion caused by hypoxia/reoxygenation.
authors.affiliation: Department of Pathophysiology, Capital University of Medical Sciences, Beijing 100069, China.
authors.forename: Xiao-wei
authors.initials: XW
authors.lastname: Qiu
authors.forename: Wen
authors.initials: W
authors.lastname: Wang
authors.forename: Dong-qiao
authors.initials: DQ
authors.lastname: Jiang
authors.forename: Hong-xia
authors.initials: HX
authors.lastname: Wang
authors.forename: Li
authors.initials: L
authors.lastname: Yan
authors.forename: Xiao-yan
authors.initials: XY
authors.lastname: Wang
authors.forename: Li-quan
authors.initials: LQ
authors.lastname: Ma
authors.forename: Ling-Qiao
authors.initials: LQ
authors.lastname: Lu
authors.forename: Chao-shu
authors.initials: CS
authors.lastname: Tang
authors.forename: Li-ke
authors.initials: LK
authors.lastname: Zhang
mesh_terms: D015126:8,11,14-Eicosatrienoic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D015687:Cell Hypoxia / Q000187:drug effects / Q000502:physiology; D002470:Cell Survival; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000187:drug effects*; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000096:biosynthesis; D052250:Nitric Oxide Synthase Type III / Q000096:biosynthesis; D015427:Reperfusion Injury / Q000517:prevention & control*; D013482:Superoxide Dismutase / Q000378:metabolism; D014471:Umbilical Veins / Q000166:cytology
chemical_list: D008315:Malondialdehyde; C046783:11,12-epoxy-5,8,14-eicosatrienoic acid; D007770:L-Lactate Dehydrogenase; D052250:Nitric Oxide Synthase Type III; D013482:Superoxide Dismutase; D048052:Mitogen-Activated Protein Kinase 3; D015126:8,11,14-Eicosatrienoic Acid