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首页> 外文期刊>The journal of sexual medicine >FK506 neuroprotection after cavernous nerve injury is mediated by thioredoxin and glutathione redox systems.
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FK506 neuroprotection after cavernous nerve injury is mediated by thioredoxin and glutathione redox systems.

机译：海绵状神经损伤后的FK506神经保护作用是由硫氧还蛋白和谷胱甘肽氧化还原系统介导的。

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INTRODUCTION: Immunophilin ligands such as FK506 (FK) preserve erectile function (EF) following cavernous nerve injury (CNI), although the precise mechanisms are unclear. We examined whether the thioredoxin (Trx) and glutathione (GSH) redox systems mediate this effect after CNI. AIM: To investigate the roles of Trx reductase 2 (TrxR2) and S-Nitrosoglutathione reductase (GSNOR) as antioxidativeitrosative and antiapoptotic mediators of the neuroprotective effect of FK in the penis after CNI. METHODS: Adult male rats, wild-type (WT) mice, and GSNOR deficient (GSNOR -/-) mice were divided into four groups: sham surgery (CN [cavernous nerves] exposure only) + vehicle; sham surgery + FK (5 mg/kg/day/rat or 2 mg/kg/day/mouse, for 2 days, subcutaneous); CNI + vehicle; and CNI + FK. At day 4 after injury, electrically stimulated changes in intracavernosal pressure (ICP) were measured. Penises were collected for Western blot analysis of TrxR2, GSNOR, and Bcl-2, and for immunolocalization of TrxR2 and GSNOR. MAIN OUTCOME MEASURES: EF assessment represented by maximal ICP and total ICP in response to electrical stimulation. Evaluation of protein expression levels and distribution patterns of antioxidativeitrosative and antiapoptotic factors in penile tissue. RESULTS: EF decreased after CNI compared with sham surgery values in both rats (P < 0.01) and WT and GSNOR -/- mice (P < 0.05). FK treatment preserved EF after CNI compared with vehicle treatment in rats (P < 0.01) and WT mice (P < 0.05) but not in GSNOR -/- mice. In rats, GSNOR (P < 0.01) and Bcl-2 (P < 0.05) expressions were significantly decreased after CNI. FK treatment in CN-injured rats restored expression of GSNOR and upregulated TrxR2 (P < 0.001) and Bcl-2 (P < 0.001) expressions compared with vehicle treatment. Localizations of proteins in the penis were observed for TrxR2 (endothelium, smooth muscle) and for GSNOR (nerves, endothelium, smooth muscle). CONCLUSIONS: The neuroprotective effect of FK in preserving EF after CNI involves antioxidativeitrosative and antiapoptotic mechanisms mediated, to some extent, by Trx and GSH systems.
机译：简介：免疫亲和素配体（如FK506（FK））在海绵状神经损伤（CNI）后可保持勃起功能（EF），尽管其确切机制尚不清楚。我们检查了CNI后，硫氧还蛋白（Trx）和谷胱甘肽（GSH）氧化还原系统是否介导了这种作用。目的：探讨Trx还原酶2（TrxR2）和S-亚硝基谷胱甘肽还原酶（GSNOR）作为FK对CNI后阴茎神经保护作用的抗氧化/亚硝化和抗凋亡介质的作用。方法：成年雄性大鼠，野生型（WT）小鼠和GSNOR缺陷型（GSNOR-/-）小鼠分为四组：假手术（仅暴露于CN（海绵体））+载体;假手术。假手术+ FK（5 mg / kg /天/大鼠或2 mg / kg /天/小鼠，连续2天，皮下注射）; CNI +车辆;和CNI + FK。受伤后第4天，测量电刺激的海绵体内压力（ICP）的变化。收集阴茎用于TrxR2，GSNOR和Bcl-2的蛋白质印迹分析，以及用于TrxR2和GSNOR的免疫定位。主要观察指标：EF评估以对电刺激的最大ICP和总ICP表示。评估阴茎组织中蛋白质表达水平以及抗氧化/亚硝化和抗凋亡因子的分布模式。结果：与假手术相比，CNI后的EF均降低（P <0.01），WT和GSNOR-/-小鼠（P <0.05）。在大鼠（P <0.01）和野生型小鼠（P <0.05）中，相比于媒介物治疗，FK治疗保留了CNI后的EF，而在GSNOR-/-小鼠中则没有。在大鼠中，CNI后GSNOR（P <0.01）和Bcl-2（P <0.05）表达明显降低。与媒介物处理相比，FK处理在CN损伤的大鼠中恢复了GSNOR的表达，并上调了TrxR2（P <0.001）和Bcl-2（P <0.001）的表达。观察到TrxR2（内皮，平滑肌）和GSNOR（神经，内皮，平滑肌）在阴茎中的蛋白质定位。结论FK对CNI维持EF的神经保护作用涉及在一定程度上由Trx和GSH系统介导的抗氧化/亚硝化和抗凋亡机制。

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