Dehydroepiandrosterone inhibits the TNF-alpha-induced inflammatory response in human umbilical vein endothelial cells

被引:49
|
作者
Gutierrez, Gisela
Mendoza, Criselda
Zapata, Estrella
Montiel, Angelica
Reyes, Elba
Montano, Luis Felipe
Lopez-Marure, Rebeca
机构
[1] Inst Nacl Cardiol Ignacio Chavez, Dept Biol Celular, Mexico City 14080, DF, Mexico
[2] Univ Nacl Autonoma Mexico, Fac Med, Dept Bioquim, Immunol Lab, Mexico City 04510, DF, Mexico
关键词
DHEA; TNF-alpha; endothelial cells; NF-kappa B; inflammation; cell adhesion;
D O I
10.1016/j.atherosclerosis.2006.02.031
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Dehydroepiandrosterone (DHEA) has a protective role against atherosclerosis. We determined the effect of pharmacological doses of DHEA upon the adhesion of monocytic U937 cells to human umbilical vein endothelial cells (HUVEC), as well as the expression of adhesion and chemoattractant molecules, the translocation of NF-KB, the degradation of IKB-alpha and the production of reactive oxygen species (ROS) in HUVEC. Adhesion of U937 cells to DHEA-treated HUVEC was evaluated by co-culture experiments using [H-3]-thymidine-labeled U937 cells. The expression of adhesion and chemoattractant molecules was evaluated by flow cytometry and RT-PCR, respectively; NF-KB translocation was determined by Electrophoretic Mobility Shift Assay (EMSA) and IKB-a degradation by Western blot. ROS production was determined by the reduction of fluorescent DCFDA. TNF-alpha was used to induce inflammatory responses in HUVEC. One hundred micromolar of DHEA-treatment inhibited the TNF-alpha-induced expression of ICAM-1, E-selectin, ROS production and U937 cells adhesion to HUVEC, and interfered with NF-KB translocation and IKB-a degradation. DHEA at the above mention concentration also inhibited the mRNA expression of MCP-1 and IL-8 in basal conditions but not in TNF-alpha-stimulated conditions. Our results suggest that DHEA inhibits the expression of molecules involved in the inflammatory process, therefore it could be used as an alternative in the treatment of chronic inflammatory diseases such as atherosclerosis. (c) 2006 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:90 / 99
页数:10
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