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Updated: Jan 7, 2026

Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
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Compound Sophorae Decoction Alleviates Ferroptosis in Colitis Rats via Activating Keap1/Nrf2/GPX4 Signaling Pathway.

Jingbo Wang1, Qianyun Chen1, Si Chu2

  • 1Department of Integrated Traditional Chinese and Western Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China, hust.edu.cn.

Gastroenterology Research and Practice
|January 1, 2026
PubMed
Summary

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The Role of AMPK Signaling in Ulcerative Colitis.

Drug design, development and therapy·2024

Compound sophorae decoction (CSD) effectively treats ulcerative colitis (UC) by reducing ferroptosis and inflammation. This study reveals CSD activates the Keap1/Nrf2/GPX4 pathway, offering a novel therapeutic mechanism for UC.

Area of Science:

  • Pharmacology
  • Gastroenterology
  • Cell Biology

Background:

  • Compound sophorae decoction (CSD) is clinically used for ulcerative colitis (UC).
  • The precise therapeutic mechanisms of CSD for UC remain unclear.
  • This study investigates CSD's efficacy and molecular mechanisms against UC.

Purpose of the Study:

  • To explore the protective effects of CSD against DSS-induced UC in rats.
  • To elucidate the molecular mechanisms underlying CSD's therapeutic action, focusing on ferroptosis.
  • To identify key active components and signaling pathways involved in CSD treatment.

Main Methods:

  • HPLC-MS/MS and TLC were used to analyze CSD constituents.
  • In vitro studies used H2O2-treated Caco-2 cells to assess CSD's impact on ferroptosis.
Keywords:
Keap1/Nrf2/GPX4 signaling pathwaycompound sophorae decoctionferroptosisulcerative colitis

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  • In vivo studies utilized a DSS-induced UC rat model to evaluate CSD's effects on inflammation, oxidative stress, and ferroptosis markers.

    • Main Results:

    • Ten main active components were identified in CSD.
    • CSD significantly reduced intestinal injury, inflammation, oxidative stress, and lipid peroxidation in DSS-treated rats.
    • CSD suppressed ferroptosis by upregulating GPX4 and SLC7A11 expression via Nrf2 pathway activation.

    Conclusions:

    • CSD ameliorates ferroptosis in DSS-induced UC rats.
    • The protective effects of CSD are mediated by the activation of the Keap1/Nrf2/GPX4 signaling pathway.
    • CSD demonstrates potential as a therapeutic agent for ulcerative colitis.