Therapeutic Effects and Mechanisms of Emodin on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice

Qingbo WANG; Ziyang QIAO; Zhiping ZHAO; Wenqi SONG; Zhiyan SI

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Qingbo WANG, Ziyang QIAO, Zhiping ZHAO, Wenqi SONG, Zhiyan SI. Therapeutic Effects and Mechanisms of Emodin on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice[J]. Journal of Kunming Medical University.

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Qingbo WANG, Ziyang QIAO, Zhiping ZHAO, Wenqi SONG, Zhiyan SI. Therapeutic Effects and Mechanisms of Emodin on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice[J]. Journal of Kunming Medical University.

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Therapeutic Effects and Mechanisms of Emodin on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice

1.
Department of General Surgery
2.
Department of Cardiology and Internal Medicine，East Campus
3.
Department of Gastroenterology，Handan Central Hospital，Handan Hebei 056001，China

Available Online: 2025-09-16

Abstract

Abstract

Objective To investigate the therapeutic effects and mechanisms of emodin （EMO） on dextran sulfate （DSS）-induced ulcerative colitis （UC） in mice. Methods DSS induced UC mouse model, detection of body weight, colon length and histopathological changes. Enzyme-linked immunosorbent assay （ELISA） was used to measure tumor necrosis factor-α （TNF-α）, interleukin-1β （IL-1β）, interleukin-6 （IL-6）, interleukin-10 （IL-10）, and myeloperoxidase （MPO） levels. Western blot analysis examined the expression of Toll-like receptor 4 （TLR4）/myeloid differentiation factor 88 （MyD88）/nuclear factor κB （NF-κB） signaling pathway-related proteins. Flow cytometry assessed the ratio of helper T cells 17 （Th17） to regulatory T cells （Treg）. Additionally, 16S rDNA sequencing was employed to evaluate gut microbiota composition. Results Compared with the normal group, DSS-treated mice exhibited significant weight loss, shortened colon length, and marked histological damage （P < 0.001）. EMO intervention, particularly at high doses, demonstrated dose-dependent improvements in body weight and colon injury （P < 0.05）. ELISA analysis showed EMO reduced TNF-α, IL-1β, and IL-6 levels while increasing IL-10 （P < 0.05）. Western blot results indicated EMO inhibited abnormal activation of the TLR4/MyD88/NF-κB pathway and restored IκB. Conclusion EMO effectively mitigates DSS-induced ulcerative colitis （UC） inflammation and intestinal damage by regulating the TLR4/MyD88/NF-κB pathway, restoring Th17/Treg balance, and maintaining microbial homeostasis, providing theoretical support for its potential as a UC therapeutic agent.
- Emodin,
- Dextran sulfate sodium,
- Ulcerative colitis,
- TLR4/MyD88/NF-κB pathway,
- Gut microbiota,
- Th17/Treg balance

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References(21)

References

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