# Plasma-activated media inhibits epithelial-mesenchymal transition and ameliorates intestinal fibrosis through the PPARγ/TGF-β1/SMAD3 pathway

## TL;DR

Plasma-activated media may help treat intestinal fibrosis by blocking a key cell transition process through a specific molecular pathway.

## Contribution

This study demonstrates that plasma-activated media inhibits intestinal fibrosis via the PPARγ/TGF-β1/SMAD3 pathway.

## Key findings

- Plasma-activated media improves intestinal fibrosis in a mouse model.
- Plasma-activated media inhibits epithelial-mesenchymal transition in intestinal cells.
- The PPARγ/TGF-β1/SMAD3 pathway is involved in the anti-fibrotic effects of plasma-activated media.

## Abstract

Inflammatory bowel disease often complicates intestinal lumen stenosis, and intestinal fibrosis is the core pathological process leading to its development. Currently, there are no effective drug treatments available to prevent or improve intestinal fibrosis. Previous studies have shown that PAM (plasma-activated media) inhibits epithelial-mesenchymal transition (EMT) and improves skin fibrosis by regulating the PPARγ/TGF-β1 axis. However, it is unclear whether PAM can improve intestinal fibrosis. We used a gradient concentration of PAM to intervene in the dextran sulfate sodium (DSS)-induced mouse intestinal fibrosis model to evaluate its effects onalleviating fibrosis and explore the specific molecular mechanisms. In addition, we used PAM to intervene in the TGF-β1-induced rat intestinal crypt epithelial cell (IEC-6) EMT and fibrosis in an in vitro model to further explore the molecular mechanisms by which PAM improves intestinal fibrosis. We found that PAM can improve intestinal fibrosis by inhibiting epithelial-mesenchymal transition through the PPARγ/TGF-β1/SMAD signaling pathway.