Dehydroepiandrosterone inhibits the activation and dysfunction of endothelial cells induced by high glucose concentration.

Abstract:

:Dehydroepiandrosterone (DHEA), an adrenal steroid, has a protective role against diabetes; however, its mechanisms of action are unknown. Here, we focus on the effect of DHEA on the activation of endothelial cells induced by a high concentration of glucose. Adhesion on U937 cells, expression of adhesion molecules, production of ROS and NO, expression of eNOS, and translocation of NF-κB were evaluated in human umbilical vein endothelial cells (HUVEC) treated with high concentrations of glucose, DHEA, or both. High concentrations of glucose (>20mM) induced an increase in adhesion, an increment in mainly E-selectin and PECAM-1 expression, as well as in ROS and NO production, eNOS expression, translocation of NF-κB, and degradation of its inhibitor IκB-α. DHEA abolished adhesion and the increase of E-selectin, ICAM-1, VCAM-1, and PECAM-1 induced by glucose. In addition, DHEA completely blocked oxidative stress and decreased translocation of NF-κB and the degradation of IκB-α induced by glucose. These results suggest that DHEA protects against the activation of endothelial cells induced by high concentrations of glucose, indicating that DHEA could be useful in the treatment of hyperglycemia and diabetes.

journal_name

Steroids

journal_title

Steroids

authors

Huerta-García E,Ventura-Gallegos JL,Victoriano ME,Montiél-Dávalos A,Tinoco-Jaramillo G,López-Marure R

doi

10.1016/j.steroids.2011.11.010

subject

Has Abstract

pub_date

2012-02-01 00:00:00

pages

233-40

issue

3

eissn

0039-128X

issn

1878-5867

pii

S0039-128X(11)00340-0

journal_volume

77

pub_type

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