ABSTRACT
Objective: To investigate the effect of Gracilaria fisheri oligosaccharides (GFO) on inflammation and colonic epithelial barrier dysfunction in colitis mice. Methods: The animals were treated by oral gavage with distilled water, 1 000 mg/kg inulin, 100, 500, or 1 000 mg/kg GFO for 14 d, or treated with 50 mg/kg mesalamine for 5 d after colitis induction (on day 10). Histopathology, inflammatory cytokines, colonic permeability, and tight junction proteins were investigated by hematoxylin and eosin staining, immunohistochemical staining, Ussing chamber technique, and Western blotting assays, respectively. Results: GFO ameliorated histological damage in colitis mice when compared to untreated colitis mice. Treatments with 100, 500, and 1 000 mg/kg GFO reduced TNF-α expression, while IL-1β was significantly reduced in colitis mice treated with 500 and 1 000 mg/kg. Compared to untreated colitis mice, GFO increased transepithelial electrical resistance, reduced fluorescein isothiocyanate-dextran paracellular flux, and modulated tight junction proteins (occludin and claudin 2) in colitis mice. Conclusions: GFO has anti-inflammatory activity and could modulate colonic epithelial barrier dysfunction in acetic acid-induced colitis mice. Furthermore, GFO could modulate the expression of tight junction proteins that play important roles in colonic barrier function.
ABSTRACT
Objective: To investigate the effect of Gracilaria fisheri oligosaccharides (GFO) on inflammation and colonic epithelial barrier dysfunction in colitis mice. Methods: The animals were treated by oral gavage with distilled water, 1 000 mg/kg inulin, 100, 500, or 1 000 mg/kg GFO for 14 d, or treated with 50 mg/kg mesalamine for 5 d after colitis induction (on day 10). Histopathology, inflammatory cytokines, colonic permeability, and tight junction proteins were investigated by hematoxylin and eosin staining, immunohistochemical staining, Ussing chamber technique, and Western blotting assays, respectively. Results: GFO ameliorated histological damage in colitis mice when compared to untreated colitis mice. Treatments with 100, 500, and 1 000 mg/kg GFO reduced TNF-α expression, while IL-1β was significantly reduced in colitis mice treated with 500 and 1 000 mg/kg. Compared to untreated colitis mice, GFO increased transepithelial electrical resistance, reduced fluorescein isothiocyanate-dextran paracellular flux, and modulated tight junction proteins (occludin and claudin 2) in colitis mice. Conclusions: GFO has anti-inflammatory activity and could modulate colonic epithelial barrier dysfunction in acetic acid-induced colitis mice. Furthermore, GFO could modulate the expression of tight junction proteins that play important roles in colonic barrier function.