The effects of estrogen like agents on cardio-protection via induction of stress proteins

性别差异是影响心脏病发病的主要因素之一。特别是在缺血性心脏病中，雌激素的抗动脉粥样硬化作用被广泛研究。然而，雌激素对心肌细胞的作用尚未阐明。因此，我们研究了17β-雌二醇对培养的心肌细胞的影响。我们利用P19CL6细胞系作为心脏祖细胞系统，并用二甲基亚砜(DMSO)诱导分化为心脏表型。17-β-雌二醇诱导分化的P19CL6细胞锰超氧化物歧化酶，增加细胞对过氧化氢的耐受性。我们还检测了176-雌二醇是否促进P19CL6细胞分化为心脏表型。与不含雌二醇的对照细胞相比，经DMSO处理的P19CL6细胞在176-雌二醇存在的情况下更早开始自发搏动。这些结果表明，17β-雌二醇通过增加心肌细胞对氧化应激的耐受性和促进祖细胞再生而对心肌细胞产生直接的心脏保护作用。

Sex difference is one of the major factors that modulate pathogenesis of heart diseases. Especially in ischemic heart diseases, anti-atherogenic actions of estrogen were examined extensively. However, the action of estrogen on cardiac myocytes per sue was not elucidated yet. Therefore, we examined the effect of 17β-estradiol on cultured cardiac myocytes. We utilized P19CL6 cell line as cardiac progenitor system and differentiated them into cardiac phenotype with DMSO. 17β-estradiol induced manganese superoxide dismutase in differentiated P19CL6 cells and increased tolerance of the cells to hydrogen peroxide. We also examined whether 176-estradiol promote differentiation of P19CL6 cells into cardiac phenotype. P19CL6 cells treated with DMSO started spontaneous beating earlier in the presence of 176-estradiol compared to control cells without estradiol. These results indicate that 17β-estradiol causes cardioprotective action directly on cardiac myocytes through the increase in the tolerance of myocytes to oxidative stress and the promotion of myocyte regeneration from progenitor cells.