Ti3C2纳米板诱导的自会破坏卵巢功能
Limei Yang1,2, Zhiting He3, Le Hu4
1Department of Obstetrics and Gynecology, Women and Children's Hospital of Chongqing Medical University, No. 120 Longshan Road, Yubei District, Chongqing, 401147, China.
Journal of nanobiotechnology
|May 12, 2024
概括
碳化 (Ti3C2) 纳米片积聚在卵巢中,导致自功能障碍和干扰卵泡发育. 这导致荷尔蒙水平的改变和潜在的女性生殖毒性.
科学领域:
- 生物医学工程 生物医学工程
- 材料科学 材料科学 材料科学
- 毒理学 毒理学 毒理学
背景情况:
- 两维超薄的Ti3C2 (MXene) 纳米片用于生物医学应用.
- 之前的研究指出,丸和胎盘中的Ti3C2积累.
- 卵巢转移和Ti3C2纳米片的损伤仍然不清楚.
研究的目的:
- 研究Ti3C2纳米板转移到卵巢的情况.
- 评估Ti3C2诱导的卵巢损伤和功能障碍.
- 阐明Ti3C2卵巢毒性的潜在机制.
主要方法:
- 建立了一个小鼠模型,用静脉注射Ti3C2纳米片注射.
- 分析了卵巢组织学,激素水平 (FSH,LH,E2,P4,T) 和自标志物 (贝克林1,ATG5,LC3II/I,P62).
- 利用KGN细胞用于体外验证自在荷尔蒙分泌中的作用.
主要成果:
- Ti3C2纳米片进入卵巢和粒粉细胞,减少毛囊数量.
- 毛囊缩小与改变的FSH,LH,E2,P4和T水平相关.
- Ti3C2通过PI3K/AKT/mTOR激活了自,导致自流阻塞和氧化应激.
- 在KGN细胞中自调节影响了雌激素和孕分泌.
结论:
- Ti3C2纳米板诱导的卵巢激素分泌是由自活化和流量损害介导的.
- 自功能障碍有助于Ti3C2诱导的卵巢颗粒细胞损伤.
- 这项研究揭示了Ti3C2诱导的女性生殖毒性的机制.
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