# Cimifugin ameliorates ulcerative colitis-related lung injury by modulating the JAK1/STAT1 signaling pathway and macrophage M1 polarization

## TL;DR

Cimifugin reduces lung damage linked to ulcerative colitis by targeting inflammation and gut-lung interactions.

## Contribution

This study demonstrates Cimifugin's novel therapeutic potential for UC-related lung injury through JAK1/STAT1 and macrophage modulation.

## Key findings

- Cimifugin ameliorates UC-related lung injury in mice by suppressing inflammation and restoring epithelial barriers.
- The compound inhibits JAK1/STAT1 signaling and M1 macrophage polarization in the colon and lungs.
- Cimifugin improves intestinal microbiota homeostasis, contributing to reduced systemic inflammation.

## Abstract

Ulcerative colitis (UC)-related lung injurys is a commonly overlooked extraintestinal manifestation and there are currently no drugs with definitive efficacy available. Cimifugin has been found to inhibit aberrant inflammation and oxidative stress, but its efficacy in UC-related lung injurys has not yet been demonstrated.

This study explored the effects of Cimifugin on UC-related lung injurys using RNA-seq in combination with 16S rRNA sequencing.

Cimifugin significantly ameliorated symptoms and attenuated colon and lung injury in a UC mouse model, restored the integrity of the intestinal and lung epithelial barriers, and suppressed lung inflammation, which was achieved by inhibiting the JAK1/STAT1 pathway and the M1 macrophage-mediated inflammatory state in the colon and lungs, as well as by improving the homeostasis of the intestinal microbiota.

Cimifugin ameliorates UC-associated lung injury by modulating the JAK1/STAT1 pathway and macrophage M1 polarization.