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进一步证明内源性硫化氢作为人及大鼠膀胱舒张的介质。

Further evidence of endogenous hydrogen sulphide as a mediator of relaxation in human and rat bladder.

机构信息

Department of Urology, Peking University First Hospital, Beijing, China.

出版信息

Asian J Androl. 2013 Sep;15(5):692-6. doi: 10.1038/aja.2013.32. Epub 2013 Jun 3.

Abstract

We investigated the expression of hydrogen sulphide (H2S) in human and rat lower urinary tract (including bladder, prostate and urethra) tissues, and we sought to determine whether H2S induces relaxation of human and Sprague-Dawley (SD) rat bladder strips. Human normal lower urinary tract tissue was obtained for the evaluation of endogenous H2S productivity using a sulphide-sensitive electrode and for the analysis of the expression levels of all three synthases of endogenous H2S, cystathionine β-synthase (CBS), cystathionine γ lyase (CSE) and 3-mercaptopyruvate sulphur transferase (MPST, as known as 3-MST) by Western blot assay. CBS, CSE and MPST were located in human sample slides by immunohistochemistry. Human and male adult SD rat bladder strips were tested for H2S function with a transducer and recorded. All experiments were repeated six times. The endogenous H2S productivity and the H2S synthases had various distributions in the human and rat lower urinary tract tissues and were located in both epithelial and stromal sections. L-cysteine (L-Cys, a substrate of CBS, CSE and MPST) elicited relaxation in a dose-dependent manner on human bladder strips pre-contracted by acetylcholine chloride. This effect could be diminished by the ATP-sensitive potassium ion (KATP) channel blocker glibenclamide (GLB), the CSE inhibitor DL-propargylglycine (PPG) and the CBS inhibitor hydroxylamine (HA). H2S and its three synthases were present in the human and rat lower urinary tract tissues and relaxed human and rat bladder strips, which implied that endogenous H2S might play a role in physiological function and pathological disorders of the lower urinary tract symptoms (LUTS) or overactive bladder (OAB).

摘要

我们研究了硫化氢(H2S)在人类和大鼠下尿路(包括膀胱、前列腺和尿道)组织中的表达,并试图确定 H2S 是否能引起人类和 Sprague-Dawley(SD)大鼠膀胱条带的松弛。我们使用硫化物敏感电极评估人类正常下尿路组织中的内源性 H2S 产生能力,并通过 Western blot 分析内源性 H2S 的三种合成酶,即胱硫醚-β-合酶(CBS)、胱硫醚-γ-裂解酶(CSE)和 3-巯基丙酮酸硫转移酶(MPST,又称 3-MST)的表达水平。CBS、CSE 和 MPST 通过免疫组织化学定位在人类样本切片中。使用换能器测试人类和成年雄性 SD 大鼠膀胱条带的 H2S 功能并记录。所有实验均重复六次。内源性 H2S 产生能力和 H2S 合成酶在人类和大鼠下尿路组织中有不同的分布,存在于上皮和基质部分。L-半胱氨酸(L-Cys,CBS、CSE 和 MPST 的底物)可引起预先用氯化乙酰胆碱收缩的人类膀胱条带的剂量依赖性松弛。这种作用可被三磷酸腺苷敏感钾离子(KATP)通道阻滞剂格列本脲(GLB)、CSE 抑制剂 DL-炔丙基甘氨酸(PPG)和 CBS 抑制剂羟胺(HA)减弱。H2S 及其三种合成酶存在于人类和大鼠的下尿路组织中,并能松弛人类和大鼠的膀胱条带,这表明内源性 H2S 可能在下尿路症状(LUTS)或过度活动膀胱(OAB)的生理功能和病理紊乱中发挥作用。

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