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

IF 4.2 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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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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葛根芩连汤加味通过调节NF-κB和Nrf2/HO-1通路改善dss诱导小鼠结肠炎。
背景:本研究旨在揭示改良葛根芩连汤(MGQD)缓解溃疡性结肠炎(UC)的潜在分子机制。方法:采用葡聚糖硫酸钠(DSS)建立C57BL/6J小鼠实验性结肠炎模型。通过测量体重、疾病活动指数(DAI)、脾脏重量、结肠长度和组织病理学特征来评价MGQD对UC小鼠的治疗作用。采用ELISA试剂盒检测白细胞介素(IL)-6、IL-1β、肿瘤坏死因子-α (TNF-α)、谷胱甘肽(GSH)、活性氧(ROS)、丙二醛(MDA)的浓度。Western blot法检测大鼠外周血中IκBα、p65、p-IκBα、p-p65、HO-1和Nrf2的表达水平。免疫荧光法检测Nrf2和p-p65蛋白水平。结果:MGQD能显著缓解小鼠结肠炎相关症状。此外,MGQD抑制UC小鼠TNF-α、IL-1β、IL-6、MDA和ROS水平,增加GSH水平。在机制上,MGQD阻止NF-κB通路的激活,同时促进Nrf2/HO-1通路的激活。结论:MGQD通过调节NF-κB和Nrf2/HO-1通路抑制炎症和氧化应激,可能是UC治疗的候选药物。
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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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