丁丁甲酸盐通过降低BMP1515的调节,通过原始卵泡激活促进中部早期青春期
Yangcheng Yao1, Wenjuan Liu2, Maoxing Tang3
1Department of Reproductive Medicine, Guangdong Women and Children Hospital, Guangzhou, China; Department of Obstetrics and Gynecology, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Ecotoxicology and environmental safety
|June 5, 2025
概括
迪布甲酸盐 (DBP) 暴露通过激活原始毛囊来加速雌性小鼠的青春期开始. 这一过程涉及BMP15/p38-MAPK/AMH通路,突出了DBP诱导的中部早期青春期 (CPP) 中的一个关键机制.
科学领域:
- 内分泌学 在内分泌学.
- 生殖生物学 生殖生物学
- 毒理学 毒理学 毒理学
背景情况:
- 双甲酸乙 (DBP) 是一种已知的内分泌干扰剂,与中部早期青春期 (CPP) 有关.
- DBP加速青春期的确切机制,特别是涉及原始卵泡激活,仍然没有被阐明.
研究的目的:
- 调查原始卵泡激活在DBP诱导的CPP中的作用.
- 探索DBP影响青春期开始和卵巢功能的分子途径.
主要方法:
- 雌性ICR幼在关键发育窗口 (PND5-PND20) 中暴露于DBP.
- 通过阴道开口评估青春期的开始;分析了HPOA轴参与和原始卵泡激活.
- 马西尼尼被用于抑制原始卵泡激活,新生儿卵巢在体外培养以研究DBP的影响.
主要成果:
- 暴露于DBP显著提升了阴道开,表明更早的青春期开始.
- DBP增加了下丘脑KISS1和GPR54的表达,并提高了血清LH和E2水平.
- 原始卵泡激活被DBP加速,这种效果被masitinib逆转;体外研究表明DBP通过BMP15/p38-MAPK通路降低AMH的调节.
结论:
- 原始毛囊激活是DBP诱导的CPP的关键调解者.
- DBP通过BMP15/p38-MAPK/AMH信号通路加速原始卵泡的激活,有助于早期的青春期.
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