Aims

In the cyclic rat in estrus, the vasoactive intestinal peptide (VIP) has an impact on ovarian function, which depends on the endocrine status of the animal. In this work, we aimed to clarify the participation of VIP in the pathophysiological condition of polycystic ovary syndrome (PCOS) using a model of PCOS induced by estradiol valerate (EV-PCOS) in rats.

Main methods

In the cyclic rat in estrus and in the EV-PCOS model, we analyzed the acute effects of blocking VIP receptors with the use of an antagonist (Ant-VIP) injected into the left or right ovarian bursa on the steroidogenic response and ovarian catecholamine levels.

Key findings

In the cyclic animal in estrus, the treatment with Ant-VIP in the left ovarian bursa resulted in a reduction in testosterone serum levels and in ovarian levels of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC), without changes in 4-hydroxy-3- methoxyphenyl (MHPG) and norepinephrine (NE). When the treatment was applied on the right side, only MHPG levels increased.

In the EV-PCOS model, the treatment with Ant-VIP in the left ovarian bursa increased testosterone, estradiol, MHPG, and NE levels. When the treatment was performed on the right side, progesterone levels decreased and estradiol increased, without changes in ovarian catecholamines.

Significance

The binding of VIP to its receptors differentially regulates steroidogenesis in the cyclic animal in estrus and in the EV-PCOS model. The blocking of VIP signaling produces changes in ovarian catecholamines.

中文翻译：

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在体内施用VIP拮抗剂可改变多囊卵巢综合征大鼠模型中卵巢激素的分泌

目的

在发情的周期性大鼠中，血管活性肠肽（VIP）对卵巢功能有影响，这取决于动物的内分泌状态。在这项工作中，我们旨在使用戊酸雌二醇（EV-PCOS）诱导的PCOS模型阐明VIP在多囊卵巢综合征（PCOS）病理生理状况中的参与。

主要方法

在发情的周期性大鼠和EV-PCOS模型中，我们通过向左或右侧卵巢囊中注射拮抗剂（Ant-VIP）分析了阻断VIP受体对类固醇生成反应和卵巢儿茶酚胺水平的急性影响。

主要发现

在发情期的周期性动物中，在左侧卵巢法氏囊中使用Ant-VIP进行治疗可降低睾丸激素血清水平以及卵巢中多巴胺和3,4-二羟基苯基乙酸（DOPAC）的水平，而4-羟基- 3-甲氧基苯基（MHPG）和去甲肾上腺素（NE）。当在右侧进行治疗时，只有MHPG水平升高。

在EV-PCOS模型中，左卵巢囊中的Ant-VIP治疗增加了睾丸激素，雌二醇，MHPG和NE的水平。当在右侧进行治疗时，孕酮水平降低而雌二醇升高，而卵巢儿茶酚胺未改变。

意义

VIP与其受体的结合在发情期和EV-PCOS模型中差异调节类固醇在周期性动物体内的生成。阻断VIP信号产生卵巢儿茶酚胺的变化。