塞斯特林2通过Keap1/Nrf2信号通路减少肠道缺血-再输液后的铁
Le-le Zhang1, Ke Ding1, Shi-Shi Liao1
1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.
Free radical biology & medicine
|February 8, 2024
概括
塞斯特林2通过Keap1/Nrf2通路减少铁亡,减轻肠道缺血-再输液损伤. 调节Sestrin2显示了对长期肠道损伤的治疗潜力.
科学领域:
- 细胞和分子生物学 细胞和分子生物学
- 胃肠病学 胃肠病学
- 病理生理学 病理生理学
背景情况:
- 斯特林是应激反应的代谢调节剂.
- 众所周知,Sestrin2可以防止多个器官的缺血-再输液 (IR) 损伤.
- 塞斯特林2在肠道缺血-再输液 (IIR) 损伤中的作用尚不清楚.
研究的目的:
- 调查Sestrin2在肠道缺血-再输液 (IIR) 损伤中的作用.
- 探索潜在的机制,包括铁和Keap1/Nrf2通路.
主要方法:
- 使用了IIR的C57BL/6J鼠标模型.
- 检查了Sestrin2表达和铁亡指标.
- 操纵了Caco-2细胞中的Sestrin2水平 (过度表达和淘汰).
主要成果:
- 塞斯特林2表达和铁位指标在IIR期间增加.
- 在Caco-2细胞中改变Sestrin2水平直接影响了铁亡.
- 塞斯特林2通过激活Keap1/Nrf2信号通路来缓解IIR诱导的铁亡.
结论:
- 塞斯特林2通过抑制铁亡作用,对IIR损伤起着保护作用.
- Keap1/Nrf2通路对于Sestrin2的保护作用至关重要.
- 塞斯特林2代表了管理IIR损伤的潜在治疗标.
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