Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, PR China.
J Trace Elem Med Biol. 2011 Jul;25(3):154-9. doi: 10.1016/j.jtemb.2011.04.001. Epub 2011 May 23.
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.
氧化应激是由硒（Se）和维生素 E（VE）联合缺乏引起的，被认为是克山病（KD）的基本因素。脱氢表雄酮（DHEA）是一种天然存在的肾上腺雄激素，具有抗氧化特性。我们发现，缺硒和 VE 的饮食会导致大鼠 KD 病变，而 0.05、0.125 和 0.25 g/kg 的 DHEA 则会导致缺硒和 VE 的大鼠左心室中氧化应激和细胞外基质（ECM）沉积的发展呈浓度依赖性抑制。此外，DHEA 还可以拮抗 NFκB 的激活，以及由缺硒和 VE 饮食引起的 TGFβ-1 和 CTGF 的随后增加。这些研究表明，DHEA 可预防氧化应激，可能对治疗硒和维生素 E 缺乏相关的 KD 有用。这些作用基于其抗氧化作用和对左心室 ECM 沉积的抑制作用。
