Hyperoside (Hyp) is a flavonoid glycoside compound that has been demonstrated to have anti-inflammatory, anti-apoptotic and antioxidant effects. However, the impact of Hyp on inflammatory bowel disease (IBD) has not been previously explored. Thus, we evaluated the role of Hyp in dextran sodium sulfate (DSS)-induced acute colitis in mice. We established a mouse model of experimental acute colitis by treating mice with drinking water supplemented with 3.0% DSS for 7 days. The disease activity index (DAI), colon length, histological features and colonic malondialdehyde (MDA) levels were examined using appropriate methods, and COX-2 expression was examined by immunohistochemistry. TNF-α, IL-4, IL-6, IL-10, NF-κB p65, Bcl-2, Bax, Caspase-3, nuclear factor-erythroid 2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1) and superoxide dismutase (SOD) levels in colorectal tissues were detected by RT-PCR and western blotting. Hyp significantly attenuated DSS-induced changes in the DAI as well as DSS-induced colonic shortening and histological changes. Hyp also inhibited inflammation, a change reflected by decreases in TNF-α, IL-6, COX-2 and NF-κB p65 expression and increases in IL-10 expression. Hyp suppressed increases in the levels of apoptosis-related proteins, such as Caspase-3 and Bax, but upregulated the level of the anti-apoptotic protein Bcl2. In addition, Hyp also exerted antioxidant effects. The MDA content was decreased, and the expression of Nrf2 and its downstream targets HO-1 and SOD were increased by Hyp. Based on these findings, Hyp possesses the ability to attenuate colitis, possibly by mitigating colonic inflammation and apoptosis via activation of the Nrf2 signaling pathway.

Eriodictyol (EDT) is a flavonoid with strong anti-inflammatory, anti-apoptotic, and antioxidant properties.To investigate the protective effect and mechanism of EDT in ulcerative colitis (UC).UC mo...

Poly(ADP‑ribose) polymerase‑1 (PARP‑1) plays a critical role in inflammatory pathways. The PARP‑1 inhibitor, 5‑aminoisoquinolinone (5‑AIQ), has been demonstrated to exert significant pharmacological effects. The present study aimed to further examine the potential mechanisms of 5‑AIQ in a mouse model of dextran sodium sulfate (DSS)‑induced colitis. Colitis conditions were assessed by changes in weight, disease activity index, colon length, histopathology and pro‑inflammatory mediators. The colonic expression of PARP/NF‑κB and STAT3 pathway components was measured by western blot analysis. Flow cytometry was used to analyze the proportion of T helper 17 cells (Th17) and regulatory T cells (Tregs) in the spleen. Western blot analysis and reverse transcription‑quantitative PCR were employed to determine the expression of the transcription factors retinoic acid‑related orphan receptor and forkhead box protein P3. The results demonstrated that 5‑AIQ reduced tissue damage and the inflammatory response in mice with experimental colitis. Moreover, 5‑AIQ increased the proportion of Treg cells and decreased the percentage of Th17 cells in the spleen. Furthermore, following 5‑AIQ treatment, the main components of the PARP/NF‑κB and STAT3 pathways were downregulated. Collectively, these results demonstrate that the PARP‑1 inhibitor, 5‑AIQ, may suppress intestinal inflammation and protect the colonic mucosa by modulating Treg/Th17 immune balance and inhibiting PARP‑1/NF‑κB and STAT3 signaling pathways in mice with experimental colitis.