睡眠不足会损害毛囊发育,这是由于S100A8 / A9驱动的巨细胞M1极化介导的花粉状细胞烧灭引起的
Qunying Fang1,2, Lei Luo1, Rentao Jin1
1Center for Reproduction and Genetics, Department of Obstetrics and Gynecology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China.
Science advances
|February 27, 2026
概括
睡眠不足会通过促进炎症和花状细胞热致死来损害卵巢功能和生育能力. 乙氨基治疗为保护生育提供了一个潜在的治疗策略.
科学领域:
- 生殖免疫学 生殖免疫学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 众所周知,睡眠剥夺 (SD) 会增加亲炎性介质.
- SD对卵巢功能和潜在机制的具体影响尚未完全理解.
研究的目的:
- 为了研究睡眠剥夺引起的卵巢损伤的免疫调节机制.
- 确定SD对卵泡发育和生育能力的影响.
- 探索SD相关生殖问题的潜在治疗干预措施.
主要方法:
- 使用雌性小鼠模型进行睡眠剥夺研究.
- 在卵巢组织上进行了批量和单细胞RNA测序.
- 进行了体内和体外实验,以验证分子通路.
- 评估毛囊发育和早期胚胎潜力.
主要成果:
- 在小鼠中,睡眠剥夺扰乱了卵泡发育,并降低了胚胎潜力.
- 在卵巢细胞中观察到的中性粒细胞 (S100a8,S100a9),M1巨分极和 pyroptosis 基因的上调.
- 证实了TLR4/Myd88/NF-κB通路的S100A8/A9激活情况.
- 这一途径诱导了M1巨细胞的两极分化和颗粒状细胞的灭.
- 乙氨基治疗减轻了SD对卵巢功能的不良影响.
结论:
- 睡眠不足会通过中性粒细胞激活,M1巨细胞两极分化和颗粒状细胞灭引起卵巢损伤.
- S100A8/A9/TLR4/Myd88/NF-κB通路是SD诱导的卵巢功能障碍的核心.
- 乙氨基显示出作为一种预防SD的生育保护策略的潜力.
- 研究结果为患有昼夜节律障碍的个体的生育能力保护提供了洞察力.
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