# Carpesium abrotanoides ethanol extract alleviates dextran sulfate sodium-induced ulcerative colitis by suppressing inflammation and apoptosis

## TL;DR

Carpesium abrotanoides extract helps reduce inflammation and tissue damage in ulcerative colitis by targeting key inflammatory and cell death pathways.

## Contribution

This study is the first to demonstrate the therapeutic potential of Carpesium abrotanoides extract in treating ulcerative colitis through multitarget mechanisms.

## Key findings

- CAE reduced disease activity and colon shortening in a mouse model of UC.
- CAE preserved intestinal barrier proteins and suppressed pro-inflammatory markers.
- CAE inhibited apoptosis by modulating Bax, Bcl-2, and caspase-3 expression.

## Abstract

Carpesium abrotanoides has been traditionally used to treat various inflammatory and infectious diseases. However, there is no scientific report on its protective activity against intestinal inflammatory disorders, including ulcerative colitis (UC). In this study, we aimed to investigate the mechanisms underlying the protective effects of C. abrotanoides extract (CAE) in UC treatment.

Key components of CAE were identified through ultra-performance liquidchromatography, and their potential targets and pathways were predicted through network pharmacology and molecular docking. The therapeutic effects of CAE were evaluated in a dextran sulfate sodium-induced UC mouse model by assessing clinical parameters, colon length, histopathology, and the expression of inflammatory, tight junction, and apoptosis-related markers.

The components of CAE, including chlorogenic acid, kaempferol 3-O-rhamnoside, 1,3-dicaffeoylquinic acid, 3,5-dicaffeoylquinic acid, and 4,5-dicaffeoylquinic acid, were identified. These components interacted with critical targets, including tumor necrosis factor, interleukin-6, interleukin-1β, caspase-3, and Bcl-2, modulating inflammatory and apoptotic pathways. In vivo experiments showed that CAE reduced the disease activity index, prevented colon shortening, and ameliorated histological damage. It preserved tight junction proteins (ZO-1 and claudin-1), reduced inflammatory cell infiltration, and downregulated pro-inflammatory mediators. Moreover, CAE inhibited the expression of the pro-apoptotic protein Bax, the execution-phase apoptotic markers cleaved caspase-3 and cleaved PARP, while upregulated the expression of the anti-apoptotic protein Bcl-2.

CAE alleviates dextran sulfate sodium-induced colitis by exerting anti-inflammatory and anti-apoptotic effects and maintaining intestinal barrier integrity. These findings support the potential of CAE as a natural multitarget therapeutic agent for UC.