Leonurine Alleviates DSS-Induced Colitis in Mice
Leonurine, an active compound derived from Leonurus japonicus, has shown significant potential in alleviating DSS-induced ulcerative colitis (UC) in mice. The study utilized a 3% dextran sulfate sodium (DSS) solution to induce colitis, replicating symptoms of human UC, including inflammation and epithelial barrier damage. Oral administration of leonurine (30 mg/kg/day) for 7 days markedly reduced symptoms such as body weight loss, colon shortening, and disease activity index (DAI) scores. Histopathological analysis revealed reduced epithelial cell loss, crypt damage, and inflammatory infiltration, improving colon tissue structure.
Leonurine enhanced intestinal barrier function by upregulating tight junction proteins claudin-1 and occludin, reducing permeability caused by DSS. ELISA tests demonstrated decreased serum levels of proinflammatory cytokines TNF-α and IL-1β, indicating its anti-inflammatory effects. Transmission electron microscopy confirmed preserved tight junction integrity, preventing structural damage caused by DSS. Transcriptomic analysis revealed 861 differentially expressed genes, with significant modulation of pathways related to leukocyte chemotaxis, extracellular matrix organization, and pancreatic secretion. Leonurine downregulated pancreatic protease genes Cela2a and Cela3b, implicated in gut inflammation and barrier disruption. Quantitative PCR validated these findings.
Leonurine also modulated gut microbiota composition, reducing inflammatory bacterial genera such as Rikenellaceae_RC9_gut_group, UBA1819, Enterococcus, and Oscillibacter. It increased the abundance of anti-inflammatory Verrucomicrobia, promoting microbial balance. By regulating pancreatic enzymes and microbial composition, leonurine restored intestinal homeostasis, limited bacterial translocation, and protected gut barrier function. These findings highlight its therapeutic potential as a natural candidate for UC treatment, warranting further research into its mechanisms in pancreatic-gut axis regulation.
