Testosterone Deficiency Causes Endothelial Dysfunction via Elevation of Asymmetric Dimethylarginine and Oxidative Stress in Castrated Rats
Testosterone Deficiency Causes Endothelial Dysfunction via Elevation of Asymmetric Dimethylarginine and Oxidative Stress in Castrated Rats
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DOI：
10.1016/j.jsxm.2017.11.001
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发表时间：
2017-12-01
影响因子：
3.5
通讯作者：
Kimura, Kazunori
中科院分区：
文献类型：
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作者：
Kataoka, Tomoya;Hotta, Yuji;Kimura, Kazunori
背景：睾酮被认为通过产生足够的一氧化氮来介导阴茎勃起反应；因此，睾酮缺乏会因一氧化氮生物利用度降低而导致勃起功能障碍。然而，睾酮缺乏时内皮功能障碍的潜在机制仍不清楚。
目的：研究睾酮缺乏大鼠模型中内皮功能障碍的机制。
方法：将大鼠分为3组：去势组（Cast）、去势并补充睾酮组（Cast + T）和假手术组（Sham）。在Cast + T组中，去势大鼠每日皮下注射睾酮（每日3mg/kg），持续4周；假手术组和去势组仅给予溶媒。
结果：术后4周进行以下检测：通过海绵体神经电刺激后测量海绵体内压和平均动脉压来评估勃起功能，通过等长张力评估内皮功能，通过超高效液相色谱 - 串联质谱法检测不对称二甲基精氨酸（ADMA）水平，以及检测炎症生物标志物的表达。
结果：在去势组中，海绵体内压与平均动脉压的比值显著降低，乙酰胆碱诱导的舒张作用减弱，血清ADMA、氧化应激和炎症生物标志物水平显著升高（P<...此处原文似乎不完整）
Background: Testosterone is believed to mediate the penile erectile response by producing adequate nitric oxide; therefore, testosterone deficiency results in erectile dysfunction through decreased nitric oxide bioavailability. However, the mechanisms underlying endothelial dysfunction in testosterone deficiency remain unclear.Aim: To investigate the mechanism of endothelial dysfunction in a rat model of testosterone deficiency.Methods: Rats were distributed into 3 groups: castrated (Cast), castrated and supplemented with testosterone (Cast thorn T), and sham (Sham). In the Cast thorn T group, castrated rats were treated daily with subcutaneous testosterone (3 mg/kg daily) for 4 weeks; Sham and Cast rats received only the vehicle.Outcomes: Erectile function using intracavernosal pressure and mean arterial pressure measurements after electrical stimulation of the cavernous nerve, endothelial function using isometric tension, asymmetric dimethylarginine (ADMA) levels using ultra-performance liquid chromatography and tandem mass spectrometry, and inflammatory biomarker expression were performed 4 weeks after the operation.Results: In the Cast group, the ratio of intracavernosal pressure to mean arterial pressure significantly decreased, acetylcholine-induced relaxation was lower, and serum ADMA, oxidative stress, and inflammation biomarker levels were significantly increased (P