在怀孕早期,B(a) P通过TRAF2-NFκB-Caspase1轴诱导卵巢颗粒细胞亡
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Hanting Xu1, Fangyuan Chen2, Zhihao Liu2
1Joint International Research Laboratory of Reproduction & Development, College of Basic Medicine, Chongqing Medical University, Chongqing 400016, PR China.
Environmental research
|April 7, 2024
概括
在怀孕初期暴露于甲 (B) 烯 (B) 导致卵巢毒性,通过TRAF2-NFκB-Caspase1通路诱导颗粒细胞的亡. 氧化应激是这种生殖毒性的关键驱动因素.
科学领域:
- 环境毒理学环境毒理学
- 生殖生物学 生殖生物学
- 细胞毒理学细胞毒理学
背景情况:
- 甲 (B) 是一种环境内分泌干扰物,与生殖毒性有关.
- 黄体 (CL) 对于胚胎植入和怀孕维持至关重要.
- 之前的研究表明B(a) P会影响胚胎植入,但其对CL功能和机制的影响尚不清楚.
研究的目的:
- 在怀孕早期研究B(a) P诱导的卵巢毒性对CL功能的影响机制.
- 为了探索氧化应激,炎症和亡在B(a) P对粒状细胞 (GCs) 的作用中的作用.
主要方法:
- 使用了一个怀孕的小鼠模型和一个体外人体颗粒细胞 (KGN) 模型.
- 小鼠被暴露于B(a) P;KGN细胞被治疗为hCG和烯-7,8-二二醇-9,10-氧化物 (BPDE),一个B(a) P代谢物.
- 评估了胚胎植入,激素水平,黄素化,氧化应激,炎症和亡.
- 通过使用抑制剂和过度表达技术,研究了TRAF2,NFκB和Caspase1信号通路的参与.
主要成果:
- 在小鼠中,B (a) P暴露减少了胚胎植入,抑制了雌激素和孕水平.
- 在KGN细胞中,BPDE损害了白质化,促进了氧化应激和炎症.
- B(a) P/BPDE诱导的亡,而不是亡,通过BID裂变通过Caspase1激活的介导.
- 抑制Caspase1,过度表达TRAF2或激活NFκB可以缓解BPDE诱导的细胞功能障碍.
结论:
- 在怀孕早期,P/BPDE通过TRAF2-NFκB-Caspase1通路诱导GC的亡,氧化应激是主要的贡献者.
- 这项研究阐明了B(a) P诱导的卵巢毒性的一种新机制,并提供了对无法解释的黄质相缺陷的见解.
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