Journal of Capital Medical University ›› 2009, Vol. 30 ›› Issue (6): 805-808.doi: 10.3969/j.issn.1006-7795.2009.06.018

• 基础研究 • Previous Articles     Next Articles

Effect of 11,12-Epoxyeicosatrienoic Acids on Injury of Endothelial Cells induced by Hypoxia/reoxygenation and ICAM-1

QIU Xiao-wei, WANG Jue, WANG Hong-xia, WANG Wen, JIANG Dong-qiao, LU Ling-qiao, TANG Chao-shu, ZHANG Li-ke   

  1. Department of Pathophysiology, School of Basic Medical Sciences, Capital Medical University
  • Received:2009-01-04 Revised:1900-01-01 Online:2009-12-21 Published:2009-12-21

Abstract: Objective To investigate the effects of 11, 12-epoxyeicosatrienoic acids(11, 12-EET) on injury of endothelial cells induced by hypoxia/reoxygenation and intercellular adhesion molecule-1(ICAM-1), and reveal the possible pathway of EETs on protection. Methods Primary cultured HUVECs were randomly divided into control group, 11, 12-EET control group, hypoxia/reoxygenation group, 11, 12-EET hypoxia/reoxygenation group. Hypoxia/reoxygenation injury model in HUVECs was produced by exposed to hypoxia(2% O2, 5% CO2 and 93% N2) for 3 hours, respectively, followed by reoxygenation(95% air and 5% CO2). The cell viability were monitored by MTT assay. Colorimetry method was used to assay methyl lnedioxyamphetamine(MDA) and activity of superoxide dismutase(SOD) in culture medium. The ICAM-1 mRNA expression was determined by reverse transcriptase-polymerase chain reaction(RT-PCR). The ICAM-1 protein expression was determined by enzyme-linked immunosorbent essay(ELISA). Western blotting method was used to detect the expression of protein kinase B(Akt). Results 11, 12-EET caused the minor injury in normal oxygen incubated HUVECs, but in hypoxia/reoxygenation HUVECs, it raised the cell viability markedly, decreased MDA content, increased the activity of SOD and the expression of Akt, and depressed the expression of ICAM-1 mRNA and protein. Conclusion 11, 12-EET may provid the protective effection against endothelial cell hypoxia/reoxygenation injury. The mechanism may be related to increasing the activity of SOD and elimination of oxygen-derived free radicals,increasing the expression of Akt, and depressing the expression of ICAM-1 mRNA and protein.

Key words: 12-EET, endothelial cell, hypoxia/reoxygenation injury

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