Carpesium abrotanoides Ethanol Extract Alleviates Dextran Sulfate Sodium-Induced Ulcerative Colitis by Suppressing Inflammation and Apoptosis

Aejin Kim¹So Yeon Kim²Kyuhyung Jo¹Eunjung Son²Chan-Sik Kim¹Dong-Seon Kim²Youn-Hwan Hwang²YUNMI LEE^2*

• ¹KM Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea
• ²KM Science Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea

Background: 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) for UC treatment. Materials and Methods: Key components of CAE were identified through ultra performance liquid chromatography, 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. Results: 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 pro-apoptotic markers (Bax, cleaved caspase-3, and PARP) and upregulated the expression of the anti-apoptotic protein Bcl-2. Conclusions: 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.