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首页> 外文期刊>The journal of sexual medicine >TNF-alpha infusion impairs corpora cavernosa reactivity.
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TNF-alpha infusion impairs corpora cavernosa reactivity.

机译：TNF-α注入会损害海绵体反应性。

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INTRODUCTION: Erectile dysfunction (ED), as well as cardiovascular diseases (CVDs), is associated with endothelial dysfunction and increased levels of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha). AIM: We hypothesized that increased TNF-alpha levels impair cavernosal function. METHODS: In vitro organ bath studies were used to measure cavernosal reactivity in mice infused with vehicle or TNF-alpha (220 ng/kg/min) for 14 days. Gene expression of nitric oxide synthase isoforms was evaluated by real-time polymerase chain reaction. MAIN OUTCOME MEASURES: Corpora cavernosa from TNF-alpha-infused mice exhibited decreased nitric oxide (NO)-dependent relaxation, which was associated with decreased endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) cavernosal expression. RESULTS: Cavernosal strips from the TNF-alpha-infused mice displayed decreased nonadrenergic-noncholinergic (NANC)-induced relaxation (59.4 +/- 6.2 vs. control: 76.2 +/- 4.7; 16 Hz) compared with the control animals. These responses were associated with decreased gene expression of eNOS and nNOS (P < 0.05). Sympathetic-mediated, as well as phenylephrine (PE)-induced, contractile responses (PE-induced contraction; 1.32 +/- 0.06 vs. control: 0.9 +/- 0.09, mN) were increased in cavernosal strips from TNF-alpha-infused mice. Additionally, infusion of TNF-alpha increased cavernosal responses to endothelin-1 and endothelin receptor A subtype (ET(A)) receptor expression (P < 0.05) and slightly decreased tumor necrosis factor-alpha receptor 1 (TNFR1) expression (P = 0.063). CONCLUSION: Corpora cavernosa from TNF-alpha-infused mice display increased contractile responses and decreased NANC nerve-mediated relaxation associated with decreased eNOS and nNOS gene expression. These changes may trigger ED and indicate that TNF-alpha plays a detrimental role in erectile function. Blockade of TNF-alpha actions may represent an alternative therapeutic approach for ED, especially in pathologic conditions associated with increased levels of this cytokine.
机译：简介：勃起功能障碍（ED）以及心血管疾病（CVD）与内皮功能障碍和促炎细胞因子（例如肿瘤坏死因子-α（TNF-alpha））水平升高相关。目的：我们假设增加的TNF-α水平会损害海绵体功能。方法：体外器官浸浴研究用于测量注入媒介物或TNF-α（220 ng / kg / min）14天的小鼠海绵体反应性。一氧化氮合酶同工型的基因表达通过实时聚合酶链反应进行评估。主要观察指标：注入TNF-α的小鼠海绵体表现出减少的一氧化氮（NO）依赖性松弛，这与内皮型一氧化氮合酶（eNOS）和神经元一氧化氮合酶（nNOS）海绵体表达减少有关。结果：与对照组相比，输注TNF-α的小鼠的海绵体膜显示出非肾上腺素-非胆碱能（NANC）诱导的松弛减少（59.4 +/- 6.2 vs.对照：76.2 +/- 4.7; 16 Hz）。这些反应与eNOS和nNOS的基因表达降低有关（P <0.05）。输注TNF-α的海绵体条带中交感介导的以及苯肾上腺素（PE）诱导的收缩反应（PE诱导的收缩; 1.32 +/- 0.06 vs.对照：0.9 +/- 0.09，mN）增加老鼠。此外，输注TNF-α增加了对内皮素1和内皮素A亚型（ET（A））受体表达的海绵体反应（P <0.05），并且肿瘤坏死因子-α受体1（TNFR1）表达略有降低（P = 0.063） ）。结论：注入TNF-α的小鼠的海绵体表现出增加的收缩反应和减少的NANC神经介导的舒张，其与减少的eNOS和nNOS基因表达有关。这些变化可能触发ED，并表明TNF-α在勃起功能中起有害作用。 TNF-α作用的阻断可能代表了ED的另一种治疗方法，特别是在与这种细胞因子水平升高相关的病理状况下。

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