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鲶鱼(胡子鲶)睾丸间质细胞睾酮分泌的内分泌调节:生长激素的可能介质

Endocrine regulation of testosterone production by Leydig cells in the catfish, Clarias batrachus: probable mediators of growth hormone.

作者信息

Nee Pathak N Dubey, Kumar Pankaj, Lal Bechan

机构信息

Department of Zoology, Banaras Hindu University, Varanasi 221 005, U.P., India.

Department of Zoology, Rajiv Gandhi University, Rono Hills, Doimukh, Itanagar 791 112, Arunachal Pradesh, India.

出版信息

Anim Reprod Sci. 2015 Mar;154:158-65. doi: 10.1016/j.anireprosci.2015.01.005. Epub 2015 Jan 28.

DOI:10.1016/j.anireprosci.2015.01.005
PMID:25650168
Abstract

Growth hormone (GH), in the recent past, has been recognized as a potent steroid stimulating hormone independent of gonadotropin (GtH). However, the mode and mechanism of its steroidogenic action in the testis is not yet elucidated, particularly in fish. The present study was designed to understand the mode and mechanism of steroidogenic action of growth hormone in testis of the catfish, Clarias batrachus through in vivo and in vitro Leydig cell culture studies using the signaling molecule inhibitors. Exogenous administration of GtH, GH and insulin to the male catfish increased testicular and circulating testosterone level. In vitro treatment of Leydig cells with these hormones also increased testosterone production. The steroidogenic action of GH appeared to be indirect and mediated through Leydig cell produced insulin-like growth factor I (IGF-I), as the treatments with actinomycin D, cycloheximide and anti-IGF-I abolished the GH-induced testosterone production by Leydig cells. The GH-induced stimulation in IGF-I production by the isolated Leydig cells further substantiates this notion. GH appears to employ cAMP/PKA and tyrosine kinase signaling pathways to induce IGF-I production, as the adenylyl cyclase inhibitor (SQ 22,536), cAMP-dependent protein kinase (PKA) blocker (H-89) and tyrosine kinase inhibitor (lavendustin A) abolished the GH-induced IGF-I production and in turn testosterone by the Leydig cells. This study suggests that GH exerts independent androgenic effect in the catfish testis indirectly through augmenting the Leydig cell production of IGF-I.

摘要

生长激素(GH)最近已被确认为一种独立于促性腺激素(GtH)的强效类固醇刺激激素。然而,其在睾丸中类固醇生成作用的方式和机制尚未阐明,尤其是在鱼类中。本研究旨在通过使用信号分子抑制剂的体内和体外莱迪希细胞培养研究,了解生长激素在鲶鱼(Clarias batrachus)睾丸中类固醇生成作用的方式和机制。向雄性鲶鱼外源施用促性腺激素、生长激素和胰岛素可提高睾丸和循环睾酮水平。用这些激素对莱迪希细胞进行体外处理也可增加睾酮的产生。生长激素的类固醇生成作用似乎是间接的,通过莱迪希细胞产生的胰岛素样生长因子I(IGF-I)介导,因为用放线菌素D、环己酰亚胺和抗IGF-I处理可消除生长激素诱导的莱迪希细胞睾酮产生。分离的莱迪希细胞中生长激素诱导的IGF-I产生刺激进一步证实了这一观点。生长激素似乎利用cAMP/PKA和酪氨酸激酶信号通路来诱导IGF-I产生,因为腺苷酸环化酶抑制剂(SQ 22,536)、cAMP依赖性蛋白激酶(PKA)阻滞剂(H-89)和酪氨酸激酶抑制剂(拉文达斯汀A)可消除生长激素诱导的IGF-I产生,进而消除莱迪希细胞产生的睾酮。本研究表明,生长激素通过增强莱迪希细胞中IGF-I的产生,间接在鲶鱼睾丸中发挥独立的雄激素作用。

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