Network Pharmacology and Multi-omics Investigation of Yiqi Huoxue Formula's Molecular Mechanisms in Treating Endometriosis

Shen D, Dongyi Shen, Panwei Hu, Hu P, Lao J, Jianting Lao, Wan Y, Yiting Wan, Hong Yang, Yang H
Combinatorial chemistry & high throughput screening · 2026 · vol. 29 · doi:10.2174/0113862073397046251115102803 · PMID:41582571 · W7125701374
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This study employed network pharmacology and multi-omics to reveal Yiqi Huoxue Formula treats endometriosis by modulating ectopic endometrial cell proliferation, invasiveness, adhesion, and apoptosis via key targets like EGFR and AKT1.

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⚙ AI-generated deep summary by qwen3.7-flash, 2026-09-23 · read from full text ⓘ

This study utilized an integrated framework of network pharmacology, transcriptomics, proteomics, and molecular biology to elucidate the therapeutic mechanisms of Yiqi Huoxue Formula (YQHXF) in treating endometriosis. The research identified 180 direct and 128 indirect targets across 19 pathways, highlighting that YQHXF modulates key cellular processes such as proliferation, invasiveness, adhesion, and apoptosis within ectopic endometrial cells. These effects were linked to specific molecular targets including EGFR, AKT1, FOS, MAPK3, and NFKB1, which regulate the associated signaling cascades. This paper is centrally about endometriosis — specifically investigating the multi-omics mechanism of a traditional Chinese medicine formula for treating the condition.

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Abstract

INTRODUCTION: Endometriosis (EMs), a prevalent disorder characterized by pelvic pain and infertility, affects numerous bodily systems and markedly diminishes life quality. Yiqi Huoxue formula (YQHXF) has demonstrated promising therapeutic efficacy. However, its active substances and underlying mechanisms remain ambiguous. METHODS: An innovative methodological framework incorporating NP, transcriptomics, proteomics, and molecular biology was utilized to investigate the active components and mechanisms of YQHXF. A network pharmacological analysis was conducted to identify the targets, biological processes, and pathways associated with YQHXF's effects on EMs. Additionally, transcriptomics, proteomics, and molecular biology techniques were applied for further mechanistic exploration at both the gene and protein levels. RESULTS: The findings suggest that YQHXF prevents EMs by modulating critical cellular processes- proliferation, invasiveness, adhesion, and apoptosis-within ectopic endometrial cells. The integration of network pharmacology, multi-omics, and molecular biology confirmed that this regulation occurs via key targets (EGFR, AKT1, FOS, MAPK3, NFKB1) and associated pathways. DISCUSSION: This study employed an integrated approach combining transcriptomics, proteomics, and molecular biology to analyze the effects of YQHXF on EMs. A total of 180 direct targets, 128 indirect targets, and 19 pathways related to YQHXF's anti-EMs effects were preliminarily identified. Based on these findings, it is proposed that YQHXF potentially achieves its remedial outcomes by influencing the proliferation, invasiveness, adhesion, and apoptosis of ectopic endometrial cells through the regulation of EGFR, AKT1, FOS, MAPK3, and NFKB1. CONCLUSION: The findings suggest that YQHXF prevents EMs by regulating critical cellular processes, including the proliferation, invasiveness, adhesion, and apoptosis of ectopic endometrial cells.
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Abstract

Introduction: Endometriosis (EMs), a prevalent disorder characterized by pelvic pain and infertility, affects numerous bodily systems and markedly diminishes life quality. Yiqi Huoxue formula (YQHXF) has demonstrated promising therapeutic efficacy. However, its active substances and underlying mechanisms remain ambiguous.

Methods

An innovative methodological framework incorporating NP, transcriptomics, proteomics, and molecular biology was utilized to investigate the active components and mechanisms of YQHXF. A network pharmacological analysis was conducted to identify the targets, biological processes, and pathways associated with YQHXF’s effects on EMs. Additionally, transcriptomics, proteomics, and molecular biology techniques were applied for further mechanistic exploration at both the gene and protein levels.

Results

The findings suggest that YQHXF prevents EMs by modulating critical cellular processes— proliferation, invasiveness, adhesion, and apoptosis—within ectopic endometrial cells. The integration of network pharmacology, multi-omics, and molecular biology confirmed that this regulation occurs via key targets (EGFR, AKT1, FOS, MAPK3, NFKB1) and associated pathways.

Discussion

This study employed an integrated approach combining transcriptomics, proteomics, and molecular biology to analyze the effects of YQHXF on EMs. A total of 180 direct targets, 128 indirect targets, and 19 pathways related to YQHXF’s anti-EMs effects were preliminarily identified. Based on these findings, it is proposed that YQHXF potentially achieves its remedial outcomes by influencing the proliferation, invasiveness, adhesion, and apoptosis of ectopic endometrial cells through the regulation of EGFR, AKT1, FOS, MAPK3, and NFKB1.

Conclusion

The findings suggest that YQHXF prevents EMs by regulating critical cellular processes, including the proliferation, invasiveness, adhesion, and apoptosis of ectopic endometrial cells.

Keywords

Network pharmacology, molecular mechanisms, multi-omics, endometriosis, treat, pelvic pain.

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endometriosisinfertility

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