# Mechanisms of Luoshi Neiyi prescription (LSNYP) in endometriosis: a network pharmacology and experimental study

## TL;DR

This study explores how Luoshi Neiyi prescription (LSNYP) works against endometriosis using network pharmacology and experiments.

## Contribution

The study combines network pharmacology and experimental validation to reveal LSNYP's molecular mechanisms in endometriosis.

## Key findings

- LSNYP targets key processes like cell migration and inflammation in endometriosis.
- Molecular docking and simulations confirmed stable interactions between LSNYP components and targets like ICAM1 and VEGFA.
- LSNYP reduced invasion and adhesion of endometriotic cells in rats and human cells.

## Abstract

Luoshi Neiyi prescription (LSNYP) is a traditional Chinese medicine that has a clinical effect on endometriosis (EMs). This study combined network pharmacology with experimental validation to explore its potential molecular mechanisms.

The primary components of LSNYP were identified based on the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and a Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine (BATMAN-TCM). The possible target proteins were predicted using the SwissTargetPrediction online tool. The GeneCards and DisGeNET databases were used to identify targets associated with EMs. The protein-protein interaction (PPI) network, herb-component-target network, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed. Molecular docking, molecular dynamics (MD) simulation and experimental verification were carried out.

217 potential therapeutic targets were identified. Enrichment analyses revealed involvement in key biological processes and pathways, including cell migration, inflammatory response, focal adhesion, and the VEGF signaling pathway, which are closely related to the adhesion-invasion-angiogenesis progression in EMs pathogenesis. Molecular docking and MD simulation results showed stable binding between corresponding components and typical targets (ICAM1, MMP9 and VEGFA) involved in the progression. Experimental results demonstrated that LSNYP could decrease typical targets of the progression in rats and inhibit the invasion, migration and adhesion capabilities of human endometriotic stromal cells (ESCs).

These findings suggest LSNYP may be a promising candidate for EMs, potentially through inhibiting the adhesion-invasion-angiogenesis progression.

The online version contains supplementary material available at 10.1186/s41065-026-00637-2.