Mechanisms of Stress-Induced Spermatogenesis Impairment in Male Rats Following Unpredictable Chronic Mild Stress (uCMS)
Mechanisms of Stress-Induced Spermatogenesis Impairment in Male Rats Following Unpredictable Chronic Mild Stress (uCMS)
复制标题
不可预测的慢性轻度应激（uCMS）后雄性大鼠应激性精子发生受损的机制
DOI：
10.3390/ijms20184470
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发表时间：
2019-09
影响因子：
5.6
通讯作者：
Sun Lei
中科院分区：
文献类型：
--
作者：
Zou Peng;Wang Xiaogang;Yang Wang;Liu Chang;Chen Qing;Yang Huan;Zhou Niya;Zeng Yingfei;Chen Hongqiang;Zhang Guowei;Liu Jinyi;Cao Jia;Ao Lin;Sun Lei
多年来，心理压力与男性生育能力之间的负相关已为人所知。本研究的目的是：(1)确定心理应激引起的大鼠生精障碍；(2)探讨糖皮质激素受体(GR)信号在这些不良反应中的作用(如果存在)。雄性SD大鼠在给予GR拮抗剂RU486(1 mg/kg/d)的同时，接受为期6周的不可预测的慢性轻度应激(UCMS)。通过睾丸病理评估、附睾精子密度、血清睾酮水平、睾丸细胞凋亡率和细胞周期进程分析来评估睾丸损伤。UCMS组大鼠血清睾酮水平降低，附睾精子密度降低。UCMS处理的大鼠精子细胞数量减少，生精小管凋亡水平增加；此外，精原细胞的细胞周期进程被阻止在G0/G1期。此外，uCMS暴露导致血清皮质酮水平升高，并激活了睾丸中的GR信号，包括GR表达上调。RU486处理抑制了GR信号转导，减轻了应激的损伤效应，导致附睾精子密度增加。总之，这项工作首次证明了GR信号的激活介导了应激诱导的生精损伤，并且这一结果与生殖细胞中的细胞凋亡和细胞周期停滞有关。
The negative association between psychological stress and male fertility has been known for many years. This study was aimed at (i) identifying spermatogenesis impairment induced by psychological stress in rats and (ii) exploring the role of glucocorticoid receptor (GR) signaling in these adverse effects (if they exist). Male Sprague Dawley rats were exposed to a six-week period of unpredictable chronic mild stress (uCMS) along with cotreatment of GR antagonist RU486 (1 mg/kg/day). Testicular damage was assessed by testicular pathological evaluation, epididymal sperm concentration, serum testosterone levels, testicular apoptotic cell measurements, and cell cycle progression analyses. Rats in the uCMS group had decreased levels of serum testosterone and decreased epididymal sperm concentration. The uCMS-treated rats also had decreased numbers of spermatids and increased levels of apoptotic seminiferous tubules; additionally, cell cycle progression of spermatogonia was arrested at the G0/G1 phase. Furthermore, uCMS exposure caused an increase in serum corticosterone level and activated GR signaling in the testes including upregulated GR expression. RU486 treatment suppressed GR signaling and alleviated the damaging effects of stress, resulting in an increased epididymal sperm concentration. Overall, this work demonstrated for the first time that the activation of GR signaling mediates stress-induced spermatogenesis impairment and that this outcome is related to cell apoptosis and cell cycle arrest in germ cells.
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影响因子：
2.9
作者：
P. Gilbeau;C. G. Smith
通讯作者：
P. Gilbeau;C. G. Smith
影响因子：
3.8
作者：
Lee DY;Kim E;Choi MH
通讯作者：
Choi MH
DOI：
--
发表时间：
2010-06
期刊：
Minerva endocrinologica
影响因子：
--
作者：
Shannon D. Whirledge;J. Cidlowski
通讯作者：
Shannon D. Whirledge;J. Cidlowski
影响因子：
--
作者：
E. Carlsen;A. Giwercman;N. Keiding;N. Skakkebæk
通讯作者：
E. Carlsen;A. Giwercman;N. Keiding;N. Skakkebæk
影响因子：
4.1
作者：
R. Schultz;J. Isola;M. Parvinen;J. Honkaniemi;A. Wikström;J. Gustafsson;M. Pelto-huikko
通讯作者：
R. Schultz;J. Isola;M. Parvinen;J. Honkaniemi;A. Wikström;J. Gustafsson;M. Pelto-huikko