【摘 要】
：
The mechanisms of cardioprotective effects of estrogen are not fully understood.Hydrogen sulfide (H2S) is generated predominantly by cystathionine γ lyase (CSE) in myocardium, and has been implicated
【机 构】
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Department of Physiology,Second Military Medical University,800 Xiangyin Road,Shanghai,China
【出 处】
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International Conference for Physiological Sciences 2012(201
论文部分内容阅读
The mechanisms of cardioprotective effects of estrogen are not fully understood.Hydrogen sulfide (H2S) is generated predominantly by cystathionine γ lyase (CSE) in myocardium, and has been implicated to have cardioprotective effects.Thus, we hypothesize that endogenous H2S contributes to the cardioprotective effects of estrogen.Neonatal cardiomyocytes of rats were isolated and cultured.The effect of 17 β-estradiol (E2) on CSE expression in cultured cardiomyocytes was examined at first.It was found that E2 treatment resulted in an increase in CSE mRNA and protein expression in a dose-dependent manner.This effect was blocked by nonselective estrogen receptor (ER) antagonist ICI 182780 and ERa antagonist MPP, but not by ERβ selective antagonist THC.Then, the role of CSE in cardioprotective effect of estrogen was investigated.E2 treatment increased cell survival,decreased caspase-3 activation and increased Akt phosphorylation in the cells upon hydrogen peroxide treatment.The protective effects of E2 were blocked by either CSE specific inhibitor PAG or knockdown of CSE expression with siRNA.Our data indicate that the cardioprotection of estrogen against oxidative stress is through, at least in part, stimulating CSE expression in cardiomyocytes.
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