Chaihuang weikuining protects against ethanol-induced gastric ulcer through modulation of gut microbiota and inhibition of JAK1/STAT3 signaling
- 1Institute of Hepatology and Epidemiology, Affiliated Hangzhou Xixi Hospital, Zhejiang Chinese Medical University
- 2School of Public Health, Zhejiang Chinese Medical University
- 3School of Basic Medical Sciences, Zhejiang Chinese Medical University
Abstract
Background: Chaihuang weikuining (CHWKN) is a traditional Chinese medicinal formula with reported anti-ulcer activity. However, the underlying mechanisms remain unclear. This study aimed to investigate the protective effects of CHWKN against ethanol-induced gastric ulcer (GU) and to explore the role of gut microbiota in mediating these effects.
Methods: An ethanol-induced GU model was established in rats. Histological staining (H&E and PAS) and biochemical analyses were used to evaluate gastric injury. Antibiotic (ABX) treatment and fecal microbiota transplantation (FMT) were performed to determine the involvement of gut microbiota. 16S rDNA sequencing was conducted to analyse microbial composition.
Results: CHWKN markedly alleviated ethanol-induced gastric mucosal injury, as evidenced by improved histopathological features and restored of gastric function. CHWKN significantly reduced myeloperoxidase (MPO) and pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, and LPS) while increasing IL-10 levels, accompanied by suppression of JAK1/STAT3 signaling. Notably, depletion of gut microbiota abolished the protective and anti-inflammatory effects of CHWKN. Conversely, FMT from CHWKN-treated donors (the donor rats treated with ethanol and CHWKN) restored gastric mucosal integrity and reduced inflammation in recipient rats. Furthermore, CHWKN remodeled the composition of gut microbiota by increasing potentially beneficial bacteria and reversing ethanol-induced dysbiosis.
Conclusion: These findings demonstrate that CHWKN exerts protective effects against ethanol-induced GU by modulating of gut microbiota and subsequently inhibiting of JAK1/STAT3 -mediated inflammation. This highlights a microbiota-dependent mechanism underlying its therapeutic action.
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BibTeX
@article{fu2026chaihuang,
title = {{Chaihuang weikuining protects against ethanol-induced gastric ulcer through modulation of gut microbiota and inhibition of JAK1/STAT3 signaling}},
author = {Ai Fu and Rui Guo and Keyi Wang and Hui Zhuge and Gaoxiang Ying and Wenjun Ma and Qinchao Ding and Songtao Li and Jianfeng Bao and Wangqin Yu},
journal = {Frontiers in Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fmicb.2026.1924725},
url = {https://www.frontiersin.org/articles/10.3389/fmicb.2026.1924725/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Chaihuang weikuining protects against ethanol-induced gastric ulcer through modulation of gut microbiota and inhibition of JAK1/STAT3 signaling
AU - Ai Fu
AU - Rui Guo
AU - Keyi Wang
AU - Hui Zhuge
AU - Gaoxiang Ying
AU - Wenjun Ma
AU - Qinchao Ding
AU - Songtao Li
AU - Jianfeng Bao
AU - Wangqin Yu
PY - 2026
DA - 2026/10/27
JO - Frontiers in Microbiology
DO - 10.3389/fmicb.2026.1924725
UR - https://www.frontiersin.org/articles/10.3389/fmicb.2026.1924725/full
AB - Background: Chaihuang weikuining (CHWKN) is a traditional Chinese medicinal formula with reported anti-ulcer activity. However, the underlying mechanisms remain unclear. This study aimed to investigate the protective effects of CHWKN against ethanol-induced gastric ulcer (GU) and to explore the role of gut microbiota in mediating these effects. Methods: An ethanol-induced GU model was established in rats. Histological staining (H&E and PAS) and biochemical analyses were used to evaluate gastric injury. Antibiotic (ABX) treatment and fecal microbiota transplantation (FMT) were performed to determine the involvement of gut microbiota. 16S rDNA sequencing was conducted to analyse microbial composition. Results: CHWKN markedly alleviated ethanol-induced gastric mucosal injury, as evidenced by improved histopathological features and restored of gastric function. CHWKN significantly reduced myeloperoxidase (MPO) and pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, and LPS) while increasing IL-10 levels, accompanied by suppression of JAK1/STAT3 signaling. Notably, depletion of gut microbiota abolished the protective and anti-inflammatory effects of CHWKN. Conversely, FMT from CHWKN-treated donors (the donor rats treated with ethanol and CHWKN) restored gastric mucosal integrity and reduced inflammation in recipient rats. Furthermore, CHWKN remodeled the composition of gut microbiota by increasing potentially beneficial bacteria and reversing ethanol-induced dysbiosis. Conclusion: These findings demonstrate that CHWKN exerts protective effects against ethanol-induced GU by modulating of gut microbiota and subsequently inhibiting of JAK1/STAT3 -mediated inflammation. This highlights a microbiota-dependent mechanism underlying its therapeutic action.
SN - 1664-302X
ER -