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image of Mechanism of Mongolian Medicine Ӧlmei-7 on Cirrhotic Ascites Using Integrated Metabolomics and Network Pharmacology

Abstract

Introduction

Ölmei-7, a traditional Mongolian medicine used for edema since the 16th century, and has remained clinically relevant. Its mechanisms for treating cirrhotic ascites are underexplored. This study integrates metabolomics and network pharmacology to elucidate these mechanisms and validates its taste properties using electronic tongue analysis.

Methods

Taste was analyzed using an electronic tongue. Bioactive components were identified HILIC UHPLC-Q-TOF MS and databases (TCMSP, GeneCards). PPI networks were built with Cytoscape and STRING, followed by GO/KEGG analyses using OmicBeans. Molecular docking was performed with OpenBabel.

Results

Electronic tongue analysis confirmed Ölmei-7’s bitter and umami tastes, aligning with Mongolian medical theory. Network pharmacology predicted 997 potential targets, 130 of which overlapped with cirrhotic-ascites-related genes. GO analysis showed enrichment in 6200 biological processes, 513 cellular components, and 784 molecular functions. KEGG analysis identified 255 pathways, including TNF and IL-17 signaling. Molecular docking of five proteins (TNF, EGFR, MMP9, JUN, BCL2) with five compounds showed stable binding, with Rutin-MMP9 at -9.1 kcal•mol-1.

Discussion

Ölmei-7’s active components (, quercetin, luteolin) likely reduce ascites by inhibiting TNF-α-mediated inflammation and vascular permeability, protecting liver function BCL2, improving fibrosis MMP9/EGFR, and reducing oxidative stress JUN. These findings support its traditional use and elucidate its mechanisms.

Conclusion

Ölmei-7 alleviates cirrhotic ascites through anti-inflammatory, antifibrotic, and antioxidative pathways, as revealed by metabolomics and network pharmacology. This study enhances understanding of its pharmacological basis and supports clinical applications.

This is an open access article published under CC BY 4.0 https://creativecommons.org/licenses/by/4.0/legalcode
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2025-10-31
2026-01-29
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