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硫化氢通过增强内皮型一氧化氮合酶的表达促进海绵体中一氧化氮的产生。

Hydrogen sulfide promotes nitric oxide production in corpus cavernosum by enhancing expression of endothelial nitric oxide synthase.

机构信息

Department of Obstetrics & Gynecology, National University Health System, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.

出版信息

Int J Impot Res. 2013 May;25(3):86-90. doi: 10.1038/ijir.2012.39. Epub 2012 Nov 22.

DOI:10.1038/ijir.2012.39
PMID:23171981
Abstract

Recently, hydrogen sulfide (H2S) has been identified as a potential therapy for ED. However, a thorough understanding of its molecular mechanisms of action would be essential to develop H2S as a new therapy for ED. In this study, the effect of H2S on nitric oxide (NO) production, especially through the expression of constitutive nitric oxide synthase (NOS) isoforms-endothelial NOS (eNOS) and neuronal NOS (nNOS) in rat corpus cavernosum (CC) were explored. Real-time PCR studies subsequent to in vitro treatment of sodium hydrosulfide hydrate (NaHS), a stable H2S donor, showed increases in eNOS but not nNOS mRNA. Western blot studies confirmed that the exogenously applied NaHS increased eNOS but not nNOS protein expression in the rat CC. Furthermore, NaHS did not alter the expressed amounts of Caveolin-1 (CAV-1), a dominant inhibitory interaction partner of eNOS, in these tissues. Not surprisingly, NaHS also enhanced the NO production in eNOS-associated membrane fraction of rat CC. Taken together, we ascertain that H2S could exert its proerectile effects by augmenting NO pathway. It appears that H2S would be particularly useful in improving the clinical outcome of ED patients, whose erectile impairment is due to an inherent attenuation of the endothelial NO formation in the cavernosum.

摘要

最近,硫化氢(H2S)已被确定为 ED 的一种潜在治疗方法。然而,要将 H2S 开发为 ED 的新疗法,深入了解其作用的分子机制至关重要。在这项研究中,研究了 H2S 对一氧化氮(NO)产生的影响,特别是通过在大鼠海绵体(CC)中表达组成型一氧化氮合酶(NOS)同工型-内皮型 NOS(eNOS)和神经元型 NOS(nNOS)。体外处理硫氢化钠(NaHS)(一种稳定的 H2S 供体)后的实时 PCR 研究显示,eNOS mRNA 增加,但 nNOS mRNA 没有增加。Western blot 研究证实,外源性应用的 NaHS 增加了大鼠 CC 中的 eNOS 但没有 nNOS 蛋白表达。此外,NaHS 并未改变这些组织中 eNOS 的主要抑制性相互作用伙伴 Caveolin-1(CAV-1)的表达量。毫不奇怪,NaHS 还增强了大鼠 CC 中与 eNOS 相关的膜部分的 NO 产生。总之,我们确定 H2S 可以通过增强 NO 途径来发挥其促勃起作用。似乎 H2S 将特别有助于改善 ED 患者的临床结果,这些患者的勃起功能障碍是由于海绵体中内皮型 NO 形成的固有减弱所致。

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