Acta Academiae Medicinae Sinica

Acta Academiae Medicinae Sinica

Acta Academiae Medicinae Sinica ›› 2006, Vol. 28 ›› Issue (6): 803-807.

• Original Articles • Previous Articles     Next Articles

Effect of 11, 12-Epoxyeicosatrienoic Acids on Hypoxia/Reoxygenation Injury in the Human Umbilical Vein Endothelial Cells

QIU Xiao-wei, WANG Wen, JIANG Dong-qiao, WANG Hong-xia, YAN Li, WANG Xiao-yan, MA Li-quan, LU ling-qiao, TANG Chao-shu, ZHANG Li-ke   

  1. Department of Pathophysiology, Capital University of Medical Sciences, Beijing 100069, China
  • Received:2006-04-28 Revised:1900-01-01 Online:2006-12-30 Published:2006-12-30
  • Contact: ZHANG Li-ke

Abstract: 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/reoxyge- nation group, inhibition of extracellular signal-regulated kinase (ERK1/2) 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.

Key words: 11,12-epoxyeicosatrienoic acids, endotdelial cell, dypoxia/reoxycenation injury