Therapeutic Effects and Mechanisms of Emodin on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice
10.12259/j.issn.2095-610X.S20250908
- VernacularTitle:大黄素对右旋糖酐硫酸钠诱导的小鼠溃疡性结肠炎的治疗作用及机制研究
- Author:
Qingbo WANG
1
;
Ziyang QIAO
;
Zhiping ZHAO
;
Wenqi SONG
;
Zhiyan SI
Author Information
1. 邯郸市中心医院普外六科,河北 邯郸 056001
- Keywords:
Emodin;
Dextran sulfate sodium;
Ulcerative colitis;
TLR4/MyD88/NF-κB pathway;
Gut microbiota;
Th17/Treg balance
- From:
Journal of Kunming Medical University
2025;46(9):72-80
- CountryChina
- Language:Chinese
-
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.
