# Integrated network pharmacology and in vivo evidence reveal vitamin E’s multi-organ protective effects in acute lung injury and secondary enteritis

## TL;DR

This study shows how vitamin E protects both the lungs and intestines during injury by targeting shared molecular pathways.

## Contribution

The study first systematically identifies 34 shared therapeutic targets linking ALI and enteritis, and demonstrates vitamin E's multi-organ protective role.

## Key findings

- Vitamin E alleviates lung pathology in an LPS-induced ALI mouse model.
- Vitamin E repairs intestinal mucosal barrier by modulating macrophage polarization and neutrophil recruitment.
- The study identifies 34 core genes shared between ALI and enteritis, revealing molecular commonalities.

## Abstract

Acute lung injury (ALI), characterized by diffuse alveolar damage and inflammation, can trigger secondary enteritis through systemic interactions, aligning with the established lung-gut axis concept—a bidirectional communication system underpinned by shared mechanisms including inflammation, oxidative stress, and barrier dysfunction; however, the molecular links remain unclear, and vitamin E’s role in this axis lacks systematic investigation.

By integrating GeneCards database screening, protein–protein interaction (PPI) network, and pathway analyses,

we identified 34 “ALI–Enteritis ∩ Vitamin E” related core genes. In an LPS-induced ALI mouse model, vitamin E alleviated lung pathology while repairing intestinal mucosal barrier through modulating M1/M2 macrophage polarization and suppressing excessive neutrophil recruitment. This study first systematically delineates molecular commonalities between ALI and enteritis, identifies 34 shared therapeutic targets, and demonstrates vitamin E’s coordinated multi-organ protection via targeting these pathways,

offering novel insights into the “lung–intestine axis” and a scientific basis for its nutritional-immunomodulatory intervention in multi-organ injury.