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通过NRF2-自途径,FGF2通过NRF2-自途径挽救了西斯普拉丁受伤的粒状细胞
Lihui Wang1, Feiyan Cheng1, Rumeng Pan1
1Department of Obstetrics and Gynecology, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710061, China.
International journal of molecular sciences
|September 28, 2023
概括
纤维细胞生长因子2 (FGF2) 通过增强核因子-红色素2相关因子2 (NRF2) 和自途径,防止化疗诱导的过早卵巢衰竭 (POF). 准NRF2为POF提供了潜在的治疗方法.
科学领域:
- 生殖生物学 生殖生物学
- 细胞生物学 细胞生物学
- 在瘤学瘤学.
背景情况:
- 过早的卵巢衰竭 (POF) 与颗粒细胞亡有关,化疗增加了青少年的发病率.
- 化疗产生的氧化应激是POF发展的关键因素,但核因子-红素2相关因子2 (NRF2) 的作用尚不清楚.
研究的目的:
- 研究NRF2在化疗引起的POF中的作用.
- 探索FGF2在受西斯白损伤的粒状细胞和POF小鼠模型中的保护机制.
主要方法:
- NRF2表达被操纵在被西斯普拉丁损伤的颗粒状细胞模型中.
- 使用拉巴胺素和氨酸调节了自性.
- 评估了FGF2对NRF2和自的作用.
- 实验在西斯胺诱导的POF小鼠模型中得到了验证.
主要成果:
- 在受西斯普拉丁损伤的细胞中,NRF2的升高不足以抵抗压力,这表明NRF2具有补偿作用.
- 通过增强自,NRF2上调保护了颗粒状细胞.
- 外源性FGF2受保护的细胞通过增加NRF2表达和核转位.
- 在小鼠模型中的发现证实了基于细胞的结果.
结论:
- 通过NRF2-自途径,FGF2通过NRF2-自途径保护受锡斯普拉丁损伤的粒状细胞.
- 向NRF2为化疗诱导的POF提供了潜在的治疗策略,特别是对于不适合FGF2治疗的患者.
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