氧化通过激活Keap1/Nrf2/HO-1信号通路来缓解mifepristone刺激的人体子宫内膜层细胞损伤
Aibing Zhu1, Fei Yao1, Mingkun Shen1
1Department of Anesthesiology, Wuxi Maternity and Child Health Care Hospital, Wuxi, China.
Immunity, inflammation and disease
|September 29, 2023
概括
氧化可以通过激活Keap1/Nrf2/HO-1通路来防止mifepristone诱导的子宫内膜损伤. 这项研究揭示了氧化在治疗女性子宫内膜损伤方面的治疗潜力.
科学领域:
- 生殖医学 生殖医学
- 细胞生物学 细胞生物学
- 疾病的分子机制.
背景情况:
- 子宫内膜损伤,通常是由炎症或内分泌疾病引起的,会影响妇女的生殖健康.
- 人体子宫内膜层细胞 (hEndoSCs) 对于维持子宫内膜恒温和修复至关重要.
- 米费普里斯诱导的HendoSC损伤作为研究子宫内膜损伤的体外模型.
研究的目的:
- 为了研究氧化对米费普里斯诱导的HendoSC损伤的保护作用.
- 阐明氧化在子宫内膜损伤中的作用背后的分子机制.
主要方法:
- 细胞活力,细胞毒性和细胞亡被评估使用MTT,LDH测定和流细胞计.
- 关键标记物的基因和蛋白质表达 (Caspase3,Keap1,Nrf2,HO-1,NQO1) 通过RT-qPCR和西白斑分析.
- 使用ELISA量化炎症性细胞因子释放.
主要成果:
- 氧化证明了保护作用,增强了HendoSC的活力,减少了亡和炎症.
- 氧化治疗增加了Keap1/Nrf2/HO-1通路蛋白的表达.
- 保护作用被ML385减弱,ML385是Keap1/Nrf2/HO-1通路的特定抑制剂.
结论:
- 在实验室中,氧化有效地减轻了mifepristone诱导的子宫内膜损伤.
- 保护机制涉及到Keap1/Nrf2/HO-1信号通路的激活.
- 氧化显示出作为治疗子宫内膜损伤的治疗剂的潜力.
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