溃疡性结肠炎
KEAP1型
医学
药理学
传统医学
化学
病理
疾病
基因
生物化学
转录因子
作者
Qiu-Shuo Ma,Qiling Chen,Guoping Wu,Yawen Yao,Yuxin Fan,Ke‐Gang Linghu,Junming Chen,Wei Xiong,Hua Yu
标识
DOI:10.3389/fphar.2025.1588525
摘要
Background: Makino (SG) - in dextran sulfate sodium (DSS)-induced UC mice. Methods: UC model was also established in NCM460 cells using lipopolysaccharide (LPS), and Caco-2 cells were used to examine intestinal mucosal integrity. Results: . Conclusion: The study reveals for the first time the differences in efficacy of different species of SH and its molecular mechanism, demonstrating that SP increases oxidative defense via the activation of the Nrf2/Keap1 pathway, therefore mitigating colitis and oxidative damage in UC mice. This discovery not only establishes a scientific foundation for the selective preference of SH species but also offers a novel technique for the creation of natural pharmaceuticals aimed at the Nrf2 pathway for the treatment of UC.
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