Modified Gegen Qinlian Decoction Ameliorates DSS-Induced Colitis in Mice via the Modulation of NF-κB and Nrf2/HO-1 Pathways.

IF 4.4 3区 医学 Q2 CELL BIOLOGY Mediators of Inflammation Pub Date : 2025-01-16 eCollection Date: 2025-01-01 DOI:10.1155/mi/7468297
Jinke Huang, Jiaqi Zhang, Zhihong Liu, Jing Ma, Yifan Wang, Fengyun Wang, Xudong Tang
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引用次数: 0

Abstract

Background: This study aims to reveal the potential molecular mechanisms of modified Gegen Qinlian decoction (MGQD) in relieving ulcerative colitis (UC). Methods: C57BL/6J mice were used to establish experimental colitis via dextran sodium sulfate (DSS). Body weight, disease activity index (DAI), spleen weight, colon length, and histopathologic features were measured to evaluate the therapeutic effects of MGQD on mice with UC. The ELISA kits were employed to assess the concentrations of interleukin (IL)-6, IL-1β, tumor necrosis factor-α (TNF-α), glutathione (GSH), reactive oxygen species (ROS), and malondialdehyde (MDA). Western blot analyses were used to assess the levels of IκBα, p65, p-IκBα, p-p65, HO-1, and Nrf2. Moreover, the protein levels of Nrf2 and p-p65 were assessed by immunofluorescence. Results: Colitis-related symptoms in mice were significantly alleviated by MGQD. Moreover, MGQD inhibited the levels of TNF-α, IL-1β, IL-6, MDA, and ROS and increased the level of GSH in mice with UC. Mechanistically, MGQD prevented the activation of the NF-κB pathway and concomitantly promoted the activation of the Nrf2/HO-1 pathway. Conclusion: MGQD alleviated UC by suppressing inflammation and oxidative stress via the modulation of NF-κB and Nrf2/HO-1 pathways, suggesting that MGQD may be a candidate therapy for UC.

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来源期刊
Mediators of Inflammation
Mediators of Inflammation 医学-免疫学
CiteScore
8.70
自引率
0.00%
发文量
202
审稿时长
4 months
期刊介绍: Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.
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