Sarcandra glabra alleviates intestinal injury via modulating gut microbiota and suppressing the IL-6/SOCS3 signaling pathway
- 1Institute of Structural Pharmacology & TCM Chemical Biology, Fujian Key Laboratory of Chinese Materia Medica, College of Pharmacy, Fujian University of Traditional Chinese Medicine
- 2Wuya College of Innovation, Key Laboratory of Structure- Based Drug Design & Discovery, Ministry of Education, Shenyang Pharmaceutical University
Abstract
Ulcerative colitis (UC) is a refractory inflammatory bowel disease characterized by gut microbiota dysbiosis and mucosal barrier disruption. Sarcandra glabra (Sg), a traditional herbal tea and dietary supplement, has been widely used to alleviate intestinal inflammation; however, its gut microbiota-dependent mechanism remains insufficiently clarified. In this study, Sg at 2, 4, and 8 g/kg was found to dose-dependently mitigate dextran sulfate sodium (DSS)-induced colitis in mice, restore mucosal barrier integrity by upregulating tight junction proteins and enhancing mucin secretion, and reduce serum levels of IL-1β, TNF-α, and IL-6. Integrative analysis of full-length 16S rRNA gene sequencing, transcriptomics, and metabolomics data revealed that Sg reshaped gut microbiota, selectively enriching Ligilactobacillus animalis while depleting Escherichia coli and Proteus vulgaris. We identified 8 microbiota-derived metabolites correlated with Ligilactobacillus animalis abundance, among which 2,3-dihydroxybenzoic acid (2,3-DHBA) exhibited the strongest protective effect against DSS-induced NCM460 cell damage. Mechanistic studies indicated that 2,3-DHBA effectively inhibited the IL-6/SOCS3 pathway and restored tight junction protein expression, effects that were reversed by exogenous IL-6. These findings demonstrate that Sg enriches for Ligilactobacillus animalis and its metabolite 2,3-DHBA, which suppresses IL-6-driven inflammation and repairs mucosal damage, supporting its potential as a microbiome-targeted dietary adjunct for UC.
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BibTeX
@article{huang2026sarcandra,
title = {{Sarcandra glabra alleviates intestinal injury via modulating gut microbiota and suppressing the IL-6/SOCS3 signaling pathway}},
author = {Shaowei Huang and Xiaomei Chi and Siting Song and Xinyi Gao and Dedian Yu and Wenbin Huang and Jiayi Wang and Lixia Chen and Hua Li},
journal = {npj Science of Food},
year = {2026},
month = jul,
doi = {10.1038/s41538-026-00968-4},
url = {https://doi.org/10.1038/s41538-026-00968-4},
note = {CC BY},
}
RIS
TY - JOUR
TI - Sarcandra glabra alleviates intestinal injury via modulating gut microbiota and suppressing the IL-6/SOCS3 signaling pathway
AU - Shaowei Huang
AU - Xiaomei Chi
AU - Siting Song
AU - Xinyi Gao
AU - Dedian Yu
AU - Wenbin Huang
AU - Jiayi Wang
AU - Lixia Chen
AU - Hua Li
PY - 2026
DA - 2026/07/01
JO - npj Science of Food
DO - 10.1038/s41538-026-00968-4
UR - https://doi.org/10.1038/s41538-026-00968-4
AB - Ulcerative colitis (UC) is a refractory inflammatory bowel disease characterized by gut microbiota dysbiosis and mucosal barrier disruption. Sarcandra glabra (Sg), a traditional herbal tea and dietary supplement, has been widely used to alleviate intestinal inflammation; however, its gut microbiota-dependent mechanism remains insufficiently clarified. In this study, Sg at 2, 4, and 8 g/kg was found to dose-dependently mitigate dextran sulfate sodium (DSS)-induced colitis in mice, restore mucosal barrier integrity by upregulating tight junction proteins and enhancing mucin secretion, and reduce serum levels of IL-1β, TNF-α, and IL-6. Integrative analysis of full-length 16S rRNA gene sequencing, transcriptomics, and metabolomics data revealed that Sg reshaped gut microbiota, selectively enriching Ligilactobacillus animalis while depleting Escherichia coli and Proteus vulgaris. We identified 8 microbiota-derived metabolites correlated with Ligilactobacillus animalis abundance, among which 2,3-dihydroxybenzoic acid (2,3-DHBA) exhibited the strongest protective effect against DSS-induced NCM460 cell damage. Mechanistic studies indicated that 2,3-DHBA effectively inhibited the IL-6/SOCS3 pathway and restored tight junction protein expression, effects that were reversed by exogenous IL-6. These findings demonstrate that Sg enriches for Ligilactobacillus animalis and its metabolite 2,3-DHBA, which suppresses IL-6-driven inflammation and repairs mucosal damage, supporting its potential as a microbiome-targeted dietary adjunct for UC.
SN - 2396-8370
ER -