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首页> 外文期刊>Cell and Tissue Research >Gonadotropin-releasing hormone analog buserelin causes neuronal loss in rat gastrointestinal tract.
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Gonadotropin-releasing hormone analog buserelin causes neuronal loss in rat gastrointestinal tract.

机译：促性腺激素释放激素类似物Buserelin导致大鼠胃肠道神经元丢失。

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摘要

Gonadotropin-releasing hormone (GnRH) analogs are given to women undergoing in vitro fertilization. Case reports describing the development of chronic intestinal pseudo-obstruction and auto-antibodies against GnRH after such treatment suggest a strong association between intestinal dysfunction and GnRH analogs. No experimental model for studying such a relationship is currently at hand. Our main goal was to investigate possible enteric neurodegeneration and titers of GnRH antibodies in response to repeated administration of the GnRH analog buserelin in rat. Rats were treated for 1-4 sessions with daily subcutaneous injections of buserelin or saline for 5 days, followed by 3 weeks of recovery. Buserelin treatment caused significant loss of submucous and myenteric neurons in the fundus, ileum, and colon. The loss of enteric neurons can, at least partly, be explained by increased apoptosis. No GnRH- or GnRH-receptor-immunoreactive (IR) enteric neurons but numerous luteinizing hormone (LH)-receptor-IR neurons were detected. After buserelin treatment, the relative number of enteric LH-receptor-IR neurons decreased, whereas that of nitric-oxide-synthase-IR neurons increased. No intestinal inflammation or increased levels of circulating interleukins/cytokines were noted in response to buserelin treatment. Serum GnRH antibody titers were undetectable or extremely low in all rats. Thus, repeated administrations of buserelin induce neurodegeneration in rat gastrointestinal tract, possibly by way of LH-receptor hyperactivation. The present findings suggest that enteric neurodegenerative effects of GnRH analog treatment in man can be mimicked in rat. However, in contrast to man, no production of GnRH auto-antibodies has been noted in rat.
机译：促性腺激素释放激素（GnRH）类似物用于接受体外受精的妇女。病例报告描述了这种治疗后慢性肠假性梗阻和针对GnRH的自身抗体的发展，这表明肠功能障碍与GnRH类似物之间有很强的联系。目前尚没有研究这种关系的实验模型。我们的主要目标是研究对大鼠重复施用GnRH类似物buserelin可能引起的肠道神经变性和GnRH抗体效价。每天皮下注射buserelin或盐水治疗大鼠1-4次，持续5天，然后恢复3周。 Buserelin治疗导致眼底，回肠和结肠的粘膜下层和肌层神经元大量丢失。肠神经元的丧失至少可以部分由凋亡增加来解释。没有检测到GnRH或GnRH受体免疫反应性（IR）肠神经元，但是检测到大量促黄体生成素（LH）-IR神经元。 Buserelin处理后，肠LH受体IR神经元的相对数量减少，而一氧化氮合酶IR神经元的相对数量增加。没有发现肠炎症或对buserelin治疗有反应的循环白介素/细胞因子水平升高。在所有大鼠中，血清GnRH抗体滴度均未检测到或极低。因此，重复施用布塞林可能导致大鼠胃肠道神经变性，可能是通过LH受体过度活化引起的。目前的发现表明，可以在大鼠中模仿GnRH类似物治疗人的肠神经退行性作用。但是，与人类相反，在大鼠中未发现GnRH自身抗体的产生。

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