• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The journal of sexual medicine >The Effects of Anti-TNF-α Antibody on Hyperprolactinemia-Related Suppression of hCG-Induced Testosterone Release in Male Rats
【24h】

The Effects of Anti-TNF-α Antibody on Hyperprolactinemia-Related Suppression of hCG-Induced Testosterone Release in Male Rats

机译：抗TNF-α抗体对雄性大鼠高泌乳素血症相关的hCG诱导的睾丸激素释放的抑制作用

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Introduction. Hyperprolactinemia (hyperPRL)-related hypogonadism or suppression of human chorionic gonadotropin (hCG)-induced testosterone (T) release is hypothesized to be mediated by a testicular interstitial macrophage and tumor necrosis factor alpha (TNF-α)-involved blockage. Aim. To test if the lower T response after hCG challenge in the hyperPRL rats is reversed by administrating anti-TNF-α antibody (Ab). Methods. HyperPRL was induced by allografting two anterior pituitary (AP) glands per rat. Control rats were grafted with similar amount of cerebral cortex. The testicular interstitial cells (TIC) were isolated from the testis 6 weeks after grafting. TIC was treated with anti-TNF-α Ab with or without hCG. The other groups of rats received intra-testicular or intra-muscular anti-TNF-α Ab 7 days before in vitro study. The TIC isolated from each testis was incubated and T release with or without hCG challenge were measured. Main Outcome Measures. Prolactin (PRL) and T were measured by radioimmunoassay. TNF-α was measured by enzyme-linked immunosorbent assay (ELISA). Results. When low dose of anti-TNF-α Ab was administered to the TIC incubation, the effects of PRL-related suppression of hCG-stimulated T release were not significant. While a higher dose of anti-TNF-α Ab almost abolished the suppressive effects of PRL to hCG-stimulated T release. Prior intra-testicular or intra-muscular administration of anti-TNF-α Ab reversed the suppressive effects of AP grafting on TIC's T release. This was demonstrated in groups with anti-TNF-α Ab injection both 7 and 1 day prior to TIC incubations. Conclusions. The data support the hypothesis that the suppression of hCG-induced T release associated with hyperPRL is through a TNF-α-mediated mechanism to suppress the Leydig cells. The effect of anti-TNF-α Ab is durable for at least 7 days. Besides intra-testicular injection, there might be other ways available for administrating Ab. Anti-TNF-α Ab has a potential therapeutic application on hyperPRL-induced hypogonadism or suppression of hCG-induced T release.
机译：介绍。高泌乳素血症（hyperPRL）相关性腺功能减退或人类绒毛膜促性腺激素（hCG）诱导的睾丸激素（T）释放的抑制被认为是由睾丸间质巨噬细胞和肿瘤坏死因子α（TNF-α）参与的阻断作用介导的。目标。为了测试在hyperPRL大鼠中hCG攻击后较低的T反应是否通过施用抗TNF-α抗体（Ab）逆转。方法。通过将每只大鼠的两个垂体前叶（AP）同种异体移植来诱导HyperPRL。对照大鼠移植了相似量的大脑皮层。移植后6周从睾丸中分离出睾丸间质细胞（TIC）。 TIC用含或不含hCG的抗TNF-αAb治疗。其他组大鼠在进行体外研究前7天接受了睾丸内或肌内抗TNF-αAb的治疗。温育从每个睾丸分离的TIC，并在有或没有hCG攻击的情况下测量T释放。主要观察指标。通过放射免疫测定法测定催乳素（PRL）和T。 TNF-α通过酶联免疫吸附测定（ELISA）测量。结果。在TIC孵育中使用低剂量的抗TNF-αAb时，PRL相关抑制hCG刺激的T释放的作用并不明显。尽管较高剂量的抗TNF-αAb几乎消除了PRL对hCG刺激的T释放的抑制作用。先前在睾丸内或肌肉内施用抗TNF-αAb可以逆转AP移植对TIC T释放的抑制作用。在TIC孵育前7天和1天用抗TNF-αAb注射的组中证明了这一点。结论。数据支持以下假设，即与hyperPRL相关的hCG诱导的T释放的抑制是通过TNF-α介导的抑制Leydig细胞的机制。抗TNF-αAb的作用至少持续7天。除睾丸内注射外，可能还有其他方法可用于Ab的给药。抗TNF-αAb在hyperPRL诱导的性腺功能低下或抑制hCG诱导的T释放方面具有潜在的治疗应用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号