The effect of DHEA treatment on the oxidative stress and myocardial fibrosis induced by Keshan disease pathogenic factors.

Abstract

Oxidative stress induced by the combined deficiencies of selenium (Se) and vitamin E (VE) is considered the basic factor of Keshan disease (KD). Dehydroepiandrosterone (DHEA) is a naturally occurring adrenal androgen that has antioxidant properties. We found that a Se- and VE-deficient diet induced KD lesions in rats, while 0.05, 0.125, and 0.25 g/kg DHEA caused a concentration-dependent inhibition in the development of oxidative stress and extracellular matrix (ECM) deposition in the left ventricles of the Se- and VE-deficient rats. In addition, DHEA counteracted activation of NFκB as well as the subsequent increase in TGFβ-1 and CTGF induced by the Se- and VE-deficient diet. These studies suggested that DHEA prevents oxidative stress and might be useful in treating Se and VE deficiency-related KD. These effects were based on its antioxidant effects and ECM deposition inhibition in left ventricles.