通过诱导Nrf2/Gpx4来抑制性结肠炎中的铁化
Jie Shi1, Shan Ji1, Mengyao Xu1
1Affiliated Huishan Hospital of Xinglin College, Nantong University, Wuxi Huishan District People's hospital, Wuxi, Jiangsu Province 214187, China.
Clinics and research in hepatology and gastroenterology
|September 23, 2024
概括
低水平与性结肠炎 (UC) 的严重程度有关. 补充剂可以通过Nrf2/Gpx4机制抑制细胞死亡途径铁亡,从而预防结肠炎.
科学领域:
- 生物化学 生化学
- 免疫学 免疫学 免疫学
- 营养科学 营养科学
背景情况:
- 是一种必不可少的微量营养素,在性结肠炎 (UC) 中具有潜在的保护作用.
- 在UC病变发生过程中的确切作用和机制尚不清楚.
- 这项研究研究了在UC中的作用.
研究的目的:
- 为了确定UC患者和健康对照者的血清水平.
- 为了探索对实验性结肠炎的治疗作用.
- 阐明作用的分子机制,重点关注铁灭菌.
主要方法:
- 在UC患者和对照人群中量化了血清水平.
- 实验性结肠炎在小鼠中被诱导使用硫酸 (DSS) 并用色素酸盐治疗.
- 细胞铁亡标志物和Nrf2/Gpx4表达被评估在体外 (Caco2细胞) 和体内.
主要成果:
- 与健康对照组相比,UC患者的血清水平较低,与疾病活动负相关.
- 治疗改善了小鼠的DSS诱导的大肠炎,并抑制了肠上皮细胞 (IEC) 铁.
- 在DSS治疗的Caco-2细胞中,抑制了铁灭菌,伴随着Nrf2/Gpx4.4的上调.
结论:
- 血清水平与UC中的肠上皮细胞费洛结有关.
- 表明对DSS诱导的大肠炎有保护作用.
- 通过上调Nrf2/Gpx4通路来抑制铁灭,这表明UC的治疗潜力.
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