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首页> 外文期刊>The journal of sexual medicine >Analysis of testosterone effects on sonic hedgehog signaling in juvenile, adolescent and adult sprague dawley rat penis.
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Analysis of testosterone effects on sonic hedgehog signaling in juvenile, adolescent and adult sprague dawley rat penis.

机译：分析睾丸激素对青少年，青少年和成年鼠疫道氏大鼠阴茎的声音刺猬信号的影响。

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INTRODUCTION: Smooth muscle apoptosis is a major contributing factor to erectile dysfunction (ED) development in prostatectomy and diabetic patients and animal models. A critical regulator of penile smooth muscle and apoptosis is Sonic hedgehog (SHH). The SHH protein is decreased in ED models and SHH treatment of cavernous nerve (CN) injured rats prevents smooth muscle apoptosis. A close association between androgen deficiency and ED has been suggested in the literature, but few studies have examined the molecular effects on penile smooth muscle and on known signaling mechanisms that regulate morphology. Aim. Examine testosterone and SHH interaction in eugonadal adult, adolescent and juvenile rats by performing castration studies and treatment with supraphysiological testosterone. METHODS: The eugonadal adult Sprague Dawley rats were either treated with testosterone for 7 or 14 days (N = 14) or were castrated for 4 or 7 days (N = 12). The juvenile rats were treated with testosterone for 8 days (N = 7). The adolescent rats were castrated and sacrificed at P88 (N = 8). The control rats had empty vehicle (N = 22) or sham surgery (N = 20). MAIN OUTCOME MEASURES: The active form of SHH protein and mRNA were quantified by semi-quantitative immunohistochemical analysis and real-time reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: Testosterone treatment did not alter SHH signaling in juvenile rats. Shh mRNA increased 3.2-fold and SHH protein increased 1.2-fold in rats castrated during puberty. In adult rats, castration decreased Shh mRNA 3.2-fold but did not alter SHH protein. Testosterone supplement in adult rats increased Shh mRNA 2.3-fold and decreased SHH protein 1.3-fold. CONCLUSIONS: SHH signaling is independent of testosterone in normal juvenile rats and is sensitive to testosterone during adolescence, while testosterone supplement in the adult adversely impacts SHH signaling in a very similar manner to that observed with CN injury.
机译：简介：平滑肌细胞凋亡是前列腺切除术，糖尿病患者和动物模型中勃起功能障碍（ED）发生的主要因素。声波刺猬（SHH）是阴茎平滑肌和细胞凋亡的关键调节剂。在ED模型中，SHH蛋白降低，SHH治疗海绵状神经（CN）损伤的大鼠可防止平滑肌细胞凋亡。在文献中已提出雄激素缺乏与ED之间的密切联系，但是很少有研究检查对阴茎平滑肌和调节形态的已知信号传导机制的分子作用。目标。通过进行去势研究和超生理学睾丸激素治疗，检查成年，成年和青少年成年雌性大鼠睾丸激素和SHH的相互作用。方法：对成年雌性Sprague Dawley大鼠进行睾丸激素治疗7或14天（N = 14），或去势4或7天（N = 12）。幼鼠用睾丸激素治疗8天（N = 7）。将青春期大鼠去势并处死于P88（N = 8）。对照大鼠空车（N = 22）或假手术（N = 20）。主要观察指标：SHH蛋白和mRNA的活性形式通过半定量免疫组化分析和实时逆转录聚合酶链反应（RT-PCR）进行定量。结果：睾丸激素治疗未改变幼年大鼠的SHH信号传导。在青春期去势的大鼠中，Shh mRNA增加3.2倍，SHH蛋白增加1.2倍。在成年大鼠中，去势使Shh mRNA降低了3.2倍，但没有改变SHH蛋白。成年大鼠补充睾丸激素可使Shh mRNA升高2.3倍，而SHH蛋白降低1.3倍。结论：在正常的幼年大鼠中，SHH信号独立于睾丸激素，并且在青春期对睾丸激素敏感，而成年睾丸激素补充剂对SHH信号的不利影响与CN损伤所观察到的非常相似。

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