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通过激活AMPK/ Nrf2通路来减轻白素诱导的肺纤维化

Xiaohua Zhang¹, Dayan Xiong², Lang Deng²

¹Department of Occupational Medicine, Hunan Prevention and Treatment Institute for Occupational Diseases, Changsha, China.

Scientific reports

|August 25, 2025

概括

通过减少肺部痕和氧化应激, 在治疗肺纤维化的过程中, 这种化合物可能为这种严重的肺病提供新的治疗途径.

科学领域:

药理学
肺病学
自然产品化学

背景情况:

异常性肺纤维化 (IPF) 是由纤维细胞激活和原沉积导致的致命肺病.
目前IPF的治疗方法有限,这凸显出需要新的治疗策略.
一种类型的黄素,已知具有抗炎和抗菌作用,但其在纤维化中的作用尚未被研究.

研究的目的:

调查Lysionotin对白血素 (BLM) 诱导的肺纤维化的抗纤维作用.
阐明Lysionotin在肺纤维化中的作用的分子机制.

主要方法:

使用白素 (BLM) 建立了小鼠肺纤维化模型.
在接受BLM治疗的小鼠中,Lysionotin是通过腹腔内注射的.
在体外研究中使用转化生长因子-β (TGF-β) 来诱导肌纤维细胞分化.

主要成果:

在小鼠中,lyssionotin治疗减轻了BLM诱导的肺纤维化.
在体外,Lysionotin抑制了TGF-β诱导的肌纤维细胞分化和氧化应激.
莱西奥激活了AMP激活蛋白激酶 (AMPK) /核因素红色素2相关因子2 (Nrf2) 途径,增加了抗氧化基因表达 (NQO-1,HO-1).

结论:

莱西奥丁具有显著的抗肺纤维化作用.
莱西奥的治疗潜力在于其通过AMPK/ Nrf2通路调节肌纤维细胞分化和氧化应激的能力.
在肺纤维化的新疗法开发中,lysionotin是一个有前途的候选药物.

关键词:

这是一个很好的机会.这种药物肌纤维细胞没有.氧化应激肺纤维化

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