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

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.