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首页> 外文期刊>The Journal of Reproduction and Development >Influence of fetal Leydig cells on the development of adult Leydig cell population in rats
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Influence of fetal Leydig cells on the development of adult Leydig cell population in rats

机译:胎儿Leydig细胞对大鼠成年Leydig细胞群体发育的影响。

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Leydig cells are the main endogenous testosterone synthesis cells in the body. Testosterone is an essential hormone in males that affects metabolism, emotion, and pubertal development. However, little is known about the development of Leydig cells and relationship between fetal Leydig cells (FLCs) and adult Leydig cells (ALCs). The aims of this study were to investigate the effect of (FLCs) on ALC development. Our study showed that FLCs in neonatal rat testis can be eliminated by 100 mg/kg ethane dimethane sulfonate (EDS) treatment without affecting the health of newborn rats. Immunohistological results showed that eliminating FLCs led to early re-generation of the ALC population (progenitor Leydig cells [PLCs] and ALCs) accompanied at first by increased and then by decreased serum testosterone, indicating that ALCs which appeared after neonatal EDS treatment were degenerated or had attenuated functions. Our results showed that FLCs were eliminated 4 days after EDS treatment, the ALC population regenerated by 21 days, and serum testosterone levels dramatically decreased at 56 days. Collectively, our results indicate that the ablation of FLCs in neonatal rat results in abnormal development of ALCs. Our study further indicates that abnormal development of Leydig cells in the fetal stage leads to steroid hormone disorders, such as testosterone deficiency, in the adult stage. Therefore, studies of Leydig cell development are important for understanding the pathogenesis of testosterone deficiency or pubertas praecox.
机译:Leydig细胞是体内主要的内源性睾丸激素合成细胞。睾丸激素是男性中必不可少的激素,会影响新陈代谢,情绪和青春期发育。但是,关于Leydig细胞的发育以及胎儿Leydig细胞(FLC)和成年Leydig细胞(ALC)之间的关系知之甚少。这项研究的目的是调查(FLCs)对ALC发展的影响。我们的研究表明,通过100 mg / kg乙烷二甲磺酸盐(EDS)处理可以消除新生大鼠睾丸中的FLC,而不会影响新生大鼠的健康。免疫组织学结果显示,消除FLC导致ALC群体(祖细胞Leydig细胞[PLC]和ALC)的早期再生,首先伴随着血清睾丸激素的升高然后降低,这表明新生儿EDS治疗后出现的ALC退化或功能减弱。我们的结果表明,EDS处理后第4天消除了FLC,第21天使ALC群体再生,而第56天血清睾丸激素水平急剧下降。总体而言,我们的结果表明,新生大鼠FLC的消融导致ALC的异常发育。我们的研究进一步表明,成年期Leydig细胞的异常发育会导致类固醇激素紊乱,例如睾丸激素缺乏症。因此,Leydig细胞发育的研究对于理解睾丸激素缺乏或pubertas praecox的发病机理很重要。

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