# Inosine, AMP, and Vidarabine: Network Pharmacology and LC-MS Reveal Key Bioactive Compounds in Periplaneta americana for Ulcerative Colitis Management

## TL;DR

This study explores how compounds in Periplaneta americana extract may help treat ulcerative colitis by reducing inflammation and promoting healing.

## Contribution

The study identifies inosine, AMP, and vidarabine as key bioactive compounds in Periplaneta americana extract for managing ulcerative colitis.

## Key findings

- Inosine, AMP, and vidarabine were found to regulate inflammation-related pathways and key targets in ulcerative colitis.
- These compounds reduced colitis symptoms in mice by suppressing pro-inflammatory markers and promoting mucosal healing.
- Molecular docking showed adenosine analogs bind to A1/A2a receptors, aiding epithelial repair and inflammation resolution.

## Abstract

Ulcerative colitis (UC) is a chronic inflammatory bowel disease with unmet therapeutic needs. This study investigates the therapeutic potential of Periplaneta americana L. extract (PAE) and its molecular mechanisms, integrating network pharmacology and experimental validation. Liquid chromatography–mass spectrometry identified 1355 compounds in PAE. Network pharmacology analysis revealed that inosine, vidarabine, and adenosine 5′-monophosphate (AMP) were core components and the core components synergistically regulated key targets and acted on inflammation-related pathways, thereby establishing a multi-target anti-inflammatory regulatory network. In vivo experiments demonstrated that these compounds significantly alleviated colitis symptoms in dextran sulfate sodium-induced mice, as evidenced by reduced disease activity index scores, preserved colonic mucosal architecture, and decreased inflammatory infiltration. Mechanistically, core compounds down-regulated granulocyte-macrophage colony-stimulating factor (GM-CSF), inducible nitric oxide synthase (iNOS)/NOS2, monocyte chemoattractant protein 1 (MCP-1), and transforming growth factor beta 1 (TGF-β1), while they up-regulated interleukin-10 (IL-10) and epidermal growth factor (EGF). Additionally, they activated epidermal growth factor receptor (EGFR)-mediated pathways. Molecular docking analysis revealed that adenosine analogs preferentially bound to A1/A2a receptors, triggering signaling cascades essential for epithelial repair and inflammation resolution. This study established the multi-component, multi-pathway mechanism of PAE in UC, highlighting its dual role in suppressing inflammation and promoting mucosal healing. By bridging traditional herbal use with modern molecular insights, these findings provided a translational foundation for developing PAE-based therapies for UC.