ArticleFrontiers in medicine2025
Homoplantaginin inhibits the progression of ulcerative colitis in mice by regulating the MMP9-RLN2 signaling axis.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by colonic mucosal inflammation and ulceration. This study investigates the therapeutic effects of homoplantaginin (Homo), a flavonoid derived from Methods: In this study, a mouse colitis model was established using DSS to assess the remission effect of Homo on colitis mice. Quantitative reverse transcription PCR (qRT-PCR) was employed to investigate the impact of Homo on intestinal mucosal barrier and pro-inflammatory cytokines in mice. The possible target genes of Homo were analyzed and screened using bioinformatics and molecular docking approaches. Microscale Thermophoresis (MST) technique was employed to examine the binding interaction between Homo and its target gene, matrix metalloproteinase 9 (MMP9). Finally, the combination of Homo and MMP9 inhibitors was utilized to verify whether Homo alleviates DSS-mediated colitis in mice through modulation of MMP9. Results: Homo (50 mg/kg) significantly alleviated colitis symptoms, lowered myeloperoxidase (MPO) activity, and improved histopathological outcomes. qRT-PCR analysis revealed that Homo inhibited the expression of pro-inflammatory cytokines (TNF- Conclusion: Homo demonstrates significant potential in alleviating colitis through targeting the MMP9-RLN2 signaling pathway, warranting further clinical investigation in UC treatment.
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