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首页> 外文期刊>The journal of sexual medicine >Inhibition of interleukin-6 attenuates erectile dysfunction in a rat model of nerve-sparing radical prostatectomy.
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Inhibition of interleukin-6 attenuates erectile dysfunction in a rat model of nerve-sparing radical prostatectomy.

机译：抑制白细胞介素6可减轻神经保留性前列腺癌根除术大鼠模型的勃起功能障碍。

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INTRODUCTION: The precise mechanisms underlying erectile dysfunction (ED) occurring after cavernous nerve (CN)-sparing surgery remain to be determined. Aim. To evaluate the expression of interleukin-6 (IL-6) and IL-6 receptor (IL-6R) after CN injury, and the effect of inhibiting IL-6 bioactivity on nerve injury-related ED. METHODS: Male Sprague-Dawley rats were divided into three groups: sham operation; bilateral CN dissection without crushing or cutting; and bilateral CN resection. In the interventional experiment, male rats underwent bilateral CN dissection, and anti-rat IL-6 antibody in phosphate-buffered saline (PBS) or vehicle alone was injected intraperitoneally immediately and 24 hours after CN dissection. MAIN OUTCOME MEASURES: One, 3, 7, 28, and 56 days after surgery, the expression of IL-6 and IL-6R in the major pelvic ganglion (MPG) was examined by real-time polymerase chain reaction. In the interventional experiment, erectile function was assessed by determining intracavernous pressure divided by arterial pressure (ICP/AP) during electrical pelvic nerve stimulation at 4 weeks after surgery in the anti-IL-6-injected rats and PBS-injected rats. The degree of nerve injury was also evaluated by retrograde dye tracing with Fluorogold. RESULTS: The expression levels of IL-6 and IL-6R were increased in the early period of CN injury, as compared with the sham group. IL-6 expression on day 1 was particularly enhanced. Four weeks after CN dissection, the anti-IL-6 group had greater ICP/AP and more FG-positive cells than the PBS group. CONCLUSIONS: Expression levels of IL-6 in the MPG were increased in the acute phase following CN injury. Inhibition of IL-6 bioactivity attenuated ED following CN dissection. Thus, the suppression of excess inflammatory responses in the acute phase may lead to improvements in ED occurring after nerve-sparing radical prostatectomy.
机译：简介：保留海绵状神经（CN）的手术后发生的勃起功能障碍（ED）的确切机制仍有待确定。目标。评估CN损伤后白介素6（IL-6）和IL-6受体（IL-6R）的表达，以及抑制IL-6生物活性对神经损伤相关ED的影响。方法：将雄性Sprague-Dawley大鼠分为三组：假手术组和假手术组。双侧CN解剖，无压伤或割伤;和双侧CN切除。在干预实验中，雄性大鼠进行了双侧CN解剖，并在CN解剖后立即和24小时内腹膜内注射了磷酸盐缓冲液（PBS）或单独溶媒中的抗大鼠IL-6抗体。主要观察指标：术后1、3、7、28和56天，采用实时聚合酶链反应检测骨盆主神经节（MPG）中IL-6和IL-6R的表达。在介入实验中，在注射抗IL-6的大鼠和注射PBS的大鼠中，在手术后4周时，通过测量骨盆神经电刺激期间的海绵体内压力除以动脉压（ICP / AP），评估勃起功能。神经损伤的程度也通过使用Fluorogold进行的染料追溯来评估。结果：与假手术组相比，CN损伤早期IL-6和IL-6R的表达水平升高。第1天的IL-6表达特别增强。 CN解剖后四周，抗IL-6组比PBS组具有更高的ICP / AP和更多的FG阳性细胞。结论：CN损伤后急性期MPG中IL-6表达水平升高。 CN解剖后，IL-6生物活性的抑制减弱了ED。因此，在急性期抑制过度的炎症反应可能会导致神经保留性前列腺癌根治术后发生ED的改善。

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