Abstract
Fargesin is a bioactive lignan from Flos Magnoliae, an herb widely used in the treatment of allergic rhinitis, sinusitis, and headache in Asia. We sought to investigate whether fargesin ameliorates experimental inflammatory bowel disease (IBD) in mice. Oral administration of fargesin significantly attenuated the symptoms of dextran sulfate sodium (DSS)-induced colitis in mice by decreasing the inflammatory infiltration and myeloperoxidase (MPO) activity, reducing tumor necrosis factor (TNF)-α secretion, and inhibiting nitric oxide (NO) production in colitis mice. The degradation of inhibitory κBα (IκBα), phosphorylation of p65, and mRNA expression of nuclear factor κB (NF-κB) target genes were inhibited by fargesin treatment in the colon of the colitis mice. In vitro, fargesin blocked the nuclear translocation of p-p65, downregulated the protein levels of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), and dose-dependently inhibited the activity of NF-κB-luciferase in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Taken together, for the first time, the current study demonstrated the anti-inflammatory effects of fargesin on chemically induced IBD might be associated with NF-κB signaling suppression. The findings may contribute to the development of therapies for human IBD by using fargesin or its derivatives.
Highlights
Inflammatory bowel disease (IBD), which generally refers to ulcerative colitis (UC) and Crohn’s disease (CD), is a progressive inflammatory condition of the gastrointestinal (GI) tract characterized by chronic and relapsing ulceration
dextran sulfate sodium (DSS)-alone treatment significantly decreased the length of the colon, and fargesin treatment reversed the reduction in colon length (Figure 1C,D)
The data showed that fargesin ameliorated the disease indexes, such as body weight loss, bloody diarrhea, colon shortening, and histological injury, in the colitis mice
Summary
Inflammatory bowel disease (IBD), which generally refers to ulcerative colitis (UC) and Crohn’s disease (CD), is a progressive inflammatory condition of the gastrointestinal (GI) tract characterized by chronic and relapsing ulceration. IBD is usually associated with severe GI symptoms including abdominal pain, diarrhea, weight loss, and rectal bleeding [1]. Current therapeutics for IBD generally include aminosalicylates, glucocorticosteroids, immunosuppressive drugs, and targeted therapies (e.g., anti-TNF antibody). Conventional therapeutics cannot prevent adverse effects, toxicity, and complications. For this reason, the development of novel and specific therapies for IBD patients is challenging and in urgent need [2]. The exact etiologies of IBD remain unknown, numerous studies have suggested that activation of the nuclear factor kappa B (NF-κB) pathway as well as excessive production of proinflammatory mediators such as nitric oxide (NO), myeloperoxidase (MPO), cyclooxygenase-2 (COX-2), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor
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