Ameliorative effect of ginsenoside Rg1 on dextran sulfate sodium-induced colitis: involvement of intestinal barrier remodeling in mice.

Abstract

Ginsenoside Rg1, a major bioactive ingredient of Panax notoginseng, has been shown to reduce gut inflammation and ameliorate experimental colitis in mice. However, it is not yet known whether it affects the intestinal barrier injury of colitis. This study explored the effect of ginsenoside Rg1 on intestinal barrier injury in dextran sulfate sodium (DSS)-induced colitis mice through an ultrastructure observation of the colonic mucosa and analysis of the expression of colonic cytoplasmatic zonula occludens-1 (ZO-1) protein. Treatment with ginsenoside Rg1, especially high-dose use, significantly ameliorated colonic histopathologic features and the severity of the colitis and reduced colonic tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ) levels and increase IL-4 levels in a mouse model of DSS-induced colitis. Its observed efficacy was comparable to that of 5-Aminosalicylic acid (5-ASA), a first-line therapeutic agent for ulcerative colitis. Notably, ginsenoside Rg1 administration was shown to up-regulate the expression of colonic ZO-1 protein, and it repaired the intestinal barrier structure in DSS-induced colitis mice. Taken together, our findings demonstrated that ginsenoside Rg1 treatment can significantly ameliorate the severity of DSS-induced colitis in mice, which involves intestinal barrier structure remodeling through lowering the levels of the colonic pro-inflammatory cytokines TNF-α and IFN-γ and increasing the anti-inflammatory cytokine IL-4. These results suggest the potential therapeutic use of ginsenoside Rg1 as a promising approach for the treatment of inflammatory bowel disease (IBD).