Wei-Mi-Shu Decoction ameliorates gastric mucosal injury in chronic gastritis with liver-stomach disharmony syndrome through the gut microbiota-hepatic bile acid metabolism axis
Abstract
IntroductionChronic gastritis (CG) is a high‐incidence disease in the digestive system, and liverstomach disharmony syndrome (LSD) is a relatively common syndrome type. This study aimed to evaluate the role and possible mechanism of traditional Chinese medicine Wei‐Mi‐Shu Decoction (WMS) in treating LSDCG.MethodsThe CG and LSDCG animal models were established and treated with WMS to observe the TCM syndrome scores and behavioral changes, histopathological alterations of the gastric mucosa, and expressions of pro‐inflammatory cytokines and tight junction proteins. Then, the changes of gut microbiota and bile acids (BAs) were analyzed by microbiota sequencing and mass spectrometry, and the protein expressions of BA receptors were detected by immunohistochemistry and WB. Finally, Lgr5‐positive (Lgr5+) gastric cells were observed by immunofluorescence staining, the expression of gastric mucosal cell differentiation markers was detected by RT‐qPCR, and the fatty acid oxidation (FAO) of Lgr5+ cells was observed by fluorescence double staining.ResultsWMS reduced the TCM syndrome scores, increased the autonomous activity ability, and improved gastric mucosal injury, inflammatory response, and gastric mucosal barrier disruption in the CG and LSDCG model rats. WMS also regulated the intestinal microbiota and BA metabolism of model rats, and promoted the levels of PPARα and RXR. In addition, WMS attenuated the loss of Lgr5+ gastric stem cells and promoted their differentiation and FAO.ConclusionIn conclusion, WMS promoted the differentiation of Lgr5+ gastric stem cells, potentially involving the gut microbiotahepatic BA metabolism axis to repair gastric mucosal injury in LSDCG.
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BibTeX
@article{zou2026weimishu,
title = {{Wei-Mi-Shu Decoction ameliorates gastric mucosal injury in chronic gastritis with liver-stomach disharmony syndrome through the gut microbiota-hepatic bile acid metabolism axis}},
author = {Xiaoyun Zou and Shouning Jia and Minmin Wei and Yongfu Qi and Hailing Li and Yan Liu and Junru Li},
journal = {Frontiers in Pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1983808},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1983808},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Wei-Mi-Shu Decoction ameliorates gastric mucosal injury in chronic gastritis with liver-stomach disharmony syndrome through the gut microbiota-hepatic bile acid metabolism axis
AU - Xiaoyun Zou
AU - Shouning Jia
AU - Minmin Wei
AU - Yongfu Qi
AU - Hailing Li
AU - Yan Liu
AU - Junru Li
PY - 2026
DA - 2026/10/30
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1983808
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.1983808
AB - IntroductionChronic gastritis (CG) is a high‐incidence disease in the digestive system, and liverstomach disharmony syndrome (LSD) is a relatively common syndrome type. This study aimed to evaluate the role and possible mechanism of traditional Chinese medicine Wei‐Mi‐Shu Decoction (WMS) in treating LSDCG.MethodsThe CG and LSDCG animal models were established and treated with WMS to observe the TCM syndrome scores and behavioral changes, histopathological alterations of the gastric mucosa, and expressions of pro‐inflammatory cytokines and tight junction proteins. Then, the changes of gut microbiota and bile acids (BAs) were analyzed by microbiota sequencing and mass spectrometry, and the protein expressions of BA receptors were detected by immunohistochemistry and WB. Finally, Lgr5‐positive (Lgr5+) gastric cells were observed by immunofluorescence staining, the expression of gastric mucosal cell differentiation markers was detected by RT‐qPCR, and the fatty acid oxidation (FAO) of Lgr5+ cells was observed by fluorescence double staining.ResultsWMS reduced the TCM syndrome scores, increased the autonomous activity ability, and improved gastric mucosal injury, inflammatory response, and gastric mucosal barrier disruption in the CG and LSDCG model rats. WMS also regulated the intestinal microbiota and BA metabolism of model rats, and promoted the levels of PPARα and RXR. In addition, WMS attenuated the loss of Lgr5+ gastric stem cells and promoted their differentiation and FAO.ConclusionIn conclusion, WMS promoted the differentiation of Lgr5+ gastric stem cells, potentially involving the gut microbiotahepatic BA metabolism axis to repair gastric mucosal injury in LSDCG.
SN - 1663-9812
ER -