通过PI3K/AKT/Nrf2通路减轻铁
Liwen Zhou1, Hanyan Xu1, Xiong Lei2
1The Key Laboratory of Interventional Pulmonology of Zhejiang Province, Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.
Journal of ethnopharmacology
|August 27, 2025
概括
通过PI3K/AKT/Nrf2通路抑制铁和炎症,来自Coptis chinensis的Coptisine (COP) 能够防止急性肺损伤 (ALI). 这凸显了COP作为肺部疾病的潜在治疗方法.
科学领域:
- 药理学
- 分子生物学
- 传统中国医学
背景情况:
- 是一种具有抗炎功能的中国传统草药.
- 科普西因 (COP) 是主要活性化合物,但其对急性肺损伤 (ALI) 的作用尚未完全理解.
研究的目的:
- 调查科普蒂辛 (COP) 对急性肺损伤 (ALI) 的保护作用.
- 阐明COP在ALI中的作用的基础分子机制.
主要方法:
- 网络药理学和RNA-seq确定了关键途径.
- 使用LPS诱导的ALI小鼠模型和基于细胞的测试 (MLE-12) 进行验证.
- 基因病理学,免疫光学和西白斑分析了治疗效果和分子变化.
主要成果:
- 在ALI小鼠中,COP治疗显著降低了肺损伤,胀和炎症.
- 通过恢复氧化回归平衡和增加抗氧化剂水平 (GSH,CAT,SOD),COP抑制了铁.
- COP激活了PI3K/AKT/Nrf2通路,上调了Nrf2,SLC7A11和GPX4等铁灭抑制剂,其作用取决于Nrf2.
结论:
- 通过激活PI3K/ AKT/ Nrf2通路,抑制炎症和铁亡,COP可以改善ALI.
- 作为临床前治疗ALI的药物,COP具有潜力.
- 向铁死是一种有效的治疗炎症性肺部疾病的策略.
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