Journal of ethnopharmacology · 2026
Wumei Wan restores the colonic mucus barrier by modulating TGF-β/Smad signaling to promote goblet cell differentiation in ulcerative colitis.
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Feng Yaqian, Chen Yangyang, Pan Mengting, Li Chi, Han Jiarong, Chen Jiani, Jiang Yanling, Ge Lilin, Chen Yuanping, Xu Shaohua, Tao Lei, Wang Qingshui, Lin Yao
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Wumei Wan (WMW), a traditional Chinese medicine formula first documented in Treatise on Febrile Diseases (Eastern Han Dynasty), was originally indicated for chronic diarrhea or dysentery. Contemporary pharmacological studies have further confirmed its definite efficacy against ulcerative colitis (UC); however, the underlying molecular mechanisms remain elusive.
AIM OF THE STUDY: Anti-inflammatory strategies fail to disrupt the "injury-immune activation-re-injury" vicious cycle in UC, rendering restoration of the epithelial barrier a promising therapeutic direction. This study centers on the classical formula WMW to systematically elucidate its molecular mechanism in ameliorating UC, with a particular focus on goblet cell fate regulation and mucus barrier restoration.
MATERIALS AND METHODS: Using a DSS-colitis model to evaluate WMW efficacy, we integrated quantitative proteomics, single-cell RNA sequencing and colonic organoids to delineate the landscape that drives goblet-cell differentiation, and identified key proteins by Western blot and immunofluorescence. UHPLC-HRMS profiling and molecular docking further provided phytochemical evidence, thereby achieving cross-scale validation from animal phenotype to cell fate.
RESULTS: WMW markedly ameliorated DSS-induced colitis and restored the mucus barrier. Proteomics and single-cell RNA-seq revealed that WMW specifically up-regulated goblet-cell core proteins, expanded the pools of mature and progenitor goblet cells, and accelerated epithelial progenitor differentiation toward this lineage. In vitro colonic organoid and cell-line assays coupled with Western blot/immunofluorescence showed that WMW inhibited TGF-β-Smad2/3 signaling, thereby activating the differentiation program.
CONCLUSION: WMW drives intestinal progenitors toward a goblet-cell fate via the TGF/Smad axis, expands the goblet-cell pool and restores the UC mucus barrier, offering a therapeutic strategy distinct from simple anti-inflammation.
AIM OF THE STUDY: Anti-inflammatory strategies fail to disrupt the "injury-immune activation-re-injury" vicious cycle in UC, rendering restoration of the epithelial barrier a promising therapeutic direction. This study centers on the classical formula WMW to systematically elucidate its molecular mechanism in ameliorating UC, with a particular focus on goblet cell fate regulation and mucus barrier restoration.
MATERIALS AND METHODS: Using a DSS-colitis model to evaluate WMW efficacy, we integrated quantitative proteomics, single-cell RNA sequencing and colonic organoids to delineate the landscape that drives goblet-cell differentiation, and identified key proteins by Western blot and immunofluorescence. UHPLC-HRMS profiling and molecular docking further provided phytochemical evidence, thereby achieving cross-scale validation from animal phenotype to cell fate.
RESULTS: WMW markedly ameliorated DSS-induced colitis and restored the mucus barrier. Proteomics and single-cell RNA-seq revealed that WMW specifically up-regulated goblet-cell core proteins, expanded the pools of mature and progenitor goblet cells, and accelerated epithelial progenitor differentiation toward this lineage. In vitro colonic organoid and cell-line assays coupled with Western blot/immunofluorescence showed that WMW inhibited TGF-β-Smad2/3 signaling, thereby activating the differentiation program.
CONCLUSION: WMW drives intestinal progenitors toward a goblet-cell fate via the TGF/Smad axis, expands the goblet-cell pool and restores the UC mucus barrier, offering a therapeutic strategy distinct from simple anti-inflammation.