黑素对低氧莱迪格细胞中基因激活蛋白激酶信号基因的影响
Mona Ghasemi1, Adel Saberivand1, Mohammadreza Gholami2
1Department of Clinical Sciences, Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran.
Veterinary research forum : an international quarterly journal
|January 16, 2025
概括
在低氧条件下,黑色素增强了小鼠莱迪格细胞中丸激素的产生. 它激活了基激活蛋白激酶 (MAPK) 途径,包括c-Jun N-终端激酶 (Jnk),P38和细胞外信号调节激酶1和2 (Erk1/2).
科学领域:
- 生殖生理学 生殖生理学
- 细胞生物学 细胞生物学
- 分子内分泌学分子内分泌学
背景情况:
- 莱迪格细胞对男性生殖至关重要;它们的功能障碍导致不孕.
- 缺氧会损害莱迪格细胞的结构和功能,影响男性的生殖健康.
- Melatonin 在应激状态下对 Leydig 细胞的保护作用需要调查.
研究的目的:
- 确定黑激素对低氧TM3小鼠莱迪格细胞中MAPK信号通路 (Jnk,P38,Erk1/2) 的影响.
- 评估黑激素对暴露于缺氧的莱迪格细胞中丸激素分泌的影响.
- 阐明黑色素潜在的保护作用背后的分子机制.
主要方法:
- TM3小鼠的莱迪格细胞暴露于由 (II) 化物 (CoCl2) 诱导的低氧.
- 定量逆转录-聚合酶连锁反应和西方布洛特分析了MAPK基因和蛋白质表达.
- 与酶相关的免疫吸收试验测量了丸激素分泌水平.
主要成果:
- 与单独的缺氧相比,黑色素治疗显著增加了的产生.
- 黑色素提高了Jnk,p38和Erk1/2.2的mRNA和蛋白质水平.
- 低氧诱导的莱迪格细胞损伤被黑激素抵消.
结论:
- 在低氧条件下,黑色素激活TM3细胞中的Jnk,p38和Erk1/2MAPK通路.
- 黑色素增强了暴露于CoCl2诱导的缺氧的莱迪格细胞中的激素的产生.
- 黑色素显示出作为男性不孕症治疗剂的潜力,与莱迪格细胞功能障碍和缺氧有关.
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