Endocrine, metabolic & immune disorders drug targets · 2026
Stigmasterol, the Active Ingredient in Huanglian Decoction, Inhibits the MAOA-NF-κB-MLCK Pathway to Improve the Inflammation in Rats With Reflux Esophagitis.
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Wang Huan, Li Lin, Han Jian, Li Yan, Yang Jun, Qiu Wangzhong, Yao Liuhua
Аннотация
OBJECTIVE: Traditional Chinese medicine (TCM) shows significant potential in treating reflux oesophagitis (RE). Huanglian Decoction (HD) is a well-known classic TCM. This study aimed to investigate the active constituents, specifically Stigmasterol and the underlying mechanisms through which HD exerts its therapeutic effects on RE.
METHODS: We employed network pharmacology, metabolomics, and molecular docking to analyze the active ingredients and interaction targets of HD and RE. An in vitro model of RE was created by incubating Het-1A cells with acidified BEBM medium. The effects of HD and Stigmasterol were evaluated by measuring cell viability, levels of inflammatory factors, and expression of tight junction proteins. Finally, the validity of the in vitro findings was confirmed by assessing the esophageal damage and inflammation in RE rats.
RESULTS: Network pharmacology has identified monoamine oxidase A (MAOA) as a core target of HD in the treatment of RE. Metabolomic analysis revealed Stigmasterol to be the active component of HD. Functional studies demonstrated that HD and Stigmasterol enhanced cell viability in acid-exposed conditions, mitigated inflammation, and increased the expression of occludin, claudin- 1, and ZO-1, while simultaneously reducing levels of p-p65, MLCK, and MAOA. Molecular docking revealed that stigmasterol binds to MAOA. Notably, the protective effect of Stigmasterol on Het-1A was negated by the overexpression of MAOA. Furthermore, in vivo studies demonstrated that HD and Stigmasterol improved acute RE in rats by inhibiting the MAOA/NF-κB-MLCK axis.
DISCUSSION: This study elucidates the role and mechanism of HD in RE. However, further clinical trials are needed to assess its applicability in clinical practice.
CONCLUSION: Stigmasterol, the active ingredient in HD, inhibits the NF-κB-MLCK pathway via MAOA, thereby reducing RE-related cellular inflammation. This research offers novel insights for RE treatment.
METHODS: We employed network pharmacology, metabolomics, and molecular docking to analyze the active ingredients and interaction targets of HD and RE. An in vitro model of RE was created by incubating Het-1A cells with acidified BEBM medium. The effects of HD and Stigmasterol were evaluated by measuring cell viability, levels of inflammatory factors, and expression of tight junction proteins. Finally, the validity of the in vitro findings was confirmed by assessing the esophageal damage and inflammation in RE rats.
RESULTS: Network pharmacology has identified monoamine oxidase A (MAOA) as a core target of HD in the treatment of RE. Metabolomic analysis revealed Stigmasterol to be the active component of HD. Functional studies demonstrated that HD and Stigmasterol enhanced cell viability in acid-exposed conditions, mitigated inflammation, and increased the expression of occludin, claudin- 1, and ZO-1, while simultaneously reducing levels of p-p65, MLCK, and MAOA. Molecular docking revealed that stigmasterol binds to MAOA. Notably, the protective effect of Stigmasterol on Het-1A was negated by the overexpression of MAOA. Furthermore, in vivo studies demonstrated that HD and Stigmasterol improved acute RE in rats by inhibiting the MAOA/NF-κB-MLCK axis.
DISCUSSION: This study elucidates the role and mechanism of HD in RE. However, further clinical trials are needed to assess its applicability in clinical practice.
CONCLUSION: Stigmasterol, the active ingredient in HD, inhibits the NF-κB-MLCK pathway via MAOA, thereby reducing RE-related cellular inflammation. This research offers novel insights for RE treatment.