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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细胞对大鼠成人Leydig细胞群的影响

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摘要

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细胞是主体中的主要内源性睾酮合成细胞。睾酮是雄性的基本激素,影响代谢,情感和青春期发育。然而,关于Leydig细胞的发育和胎儿Leydig细胞(FLC)和成人leydig细胞(ALC)之间的关系很少。本研究的目的是探讨(FLCS)对ALC发育的影响。我们的研究表明,新生大鼠睾丸的FLC可以通过100mg / kg乙烷二甲烷磺酸盐(EDS)治疗来消除,而不会影响新生大鼠的健康。免疫组织学结果表明,消除FLC导致ALC群体的早期重新产生(祖细胞[PLCS]和ALC),首先通过增加,然后通过降低的血清睾酮,表明新生儿EDS治疗后出现的ALC是退化的有衰减的功能。我们的研究结果表明,EDS治疗后4天消除了FLC,在21天内再生的ALC人群,血清睾酮水平在56天内显着降低。集体,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,胎儿阶段中Leydig细胞的异常发育导致成人阶段的类固醇激素紊乱,例如睾酮缺乏症。因此,Leydig细胞发育的研究对于了解睾酮缺乏或蒲浴蛋白的发病机制是重要的。

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