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    Genistein Alleviates Dextran Sulfate Sodiuminduced Ulcerative Colitis in Mice by Regulating Th17/Treg Cell Balance: Implication for the G Protein-coupled Estrogen Receptor

    Baolian Shu1, Youxing Wu1, Xiaoyang Wang1, Jianlan Hu1, Danxia Zhang1, Xianghao Gong2, Saiqi He3, Yangzhi Xie4, Xuan Chen4, Ruohu Gui1★★ Corresponding author

    1. 1Department of Gastroenterology, The Central Hospital of Hengyang City, Hengyang, Hunan, CHINA.
    2. 2Department of Medical Oncology, The Central Hospital of Hengyang City, Hengyang, Hunan, CHINA.
    3. 3Department of General Surgery, The Central Hospital of Hengyang City, Hengyang, Hunan, CHINA.
    4. 4Department of Neuroscience, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.

    CORRESPONDENCE

    Ruohu Gui

    Department of Gastroenterology, The Central Hospital of Hengyang City, Hengyang, Hunan, CHINA.

    18075873080@163.com

    Received: 09-08-2023; Accepted: 10-11-2023.

    Volume 20, Issue 2 · pp. 676–685 · PUBLISHED 2024 · DOI: 10.1177/09731296231217599

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Objectives: This study aimed to evaluate the therapeutic effects and mechanism of genistein on dextran sulfate sodiuminduced mouse model of ulcerative colitis (UC). Materials and Methods: A DSS-induced mouse model for UC was used in this study. Mice were then treated with genistein or a combination of genistein and the G protein-coupled estrogen receptor (GPER) antagonist G15. Colon length, disease activity index (DAI), spleen index (SI), histopathological alterations, and integrity of the colonic barrier were evaluated. The expression of inflammatory cytokines and antioxidant capacity were detected. Populations of T helper 17 cells (Th17) and Regulatory T cells (Treg) in the mesenteric lymph nodes (MLN) were analyzed. The expression of a transcription factor for Th17 and Treg in the colonic tissues was detected. Results: Genistein treatment significantly alleviated DSS-induced colitis, summarized as increased colonic length, decreased DAI, SI, improved histopathological alterations, and colonic barrier integrity. Genistein treatment restrained pro-inflammatory cytokines and oxidative enzyme release while promoting anti-inflammatory and anti-oxidative enzyme release. Flow cytometry indicated that genistein significantly reduced the Th17 population while boosting Treg populations. Furthermore, genistein inhibited the expression of transcription factors associated with Th17 and promoted the expression of transcription factors associated with Treg in the colonic tissue. Intriguingly, these observed effects of genistein were abolished when UC mice were treated with a combination of genistein and GPER antagonist G15. Conclusion: This study suggests that genistein is potent in protecting against DSS-induced colonic injuries by rebalancing Th17/Treg and that GPER may be a vital target for genistein-mediated immunomodulatory effects in UC.

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      Shu, B., Wu, Y., Wang, X., Hu, J., Zhang, D., Gong, X., He, S., Xie, Y., Chen, X., & Gui, R. (2024). Genistein Alleviates Dextran Sulfate Sodiuminduced Ulcerative Colitis in Mice by Regulating Th17/Treg Cell Balance: Implication for the G Protein-coupled Estrogen Receptor. Pharmacognosy Magazine, 20(2), 676–685. https://doi.org/10.1177/09731296231217599