Abstract
The polyphenolic compound 2,3,5,4′-tetrahydroxystilbene-2-O-beta-D-glucoside (THSG) has been shown to possess anti-inflammatory effects. Here, we examined the effects of THSG on experimental mice with colitis induced by acetic acid and whether the underlying mechanisms were associated with the PPAR-γ and NF-κB pathways. Mice were randomized into six equal groups: normal, colitis model, THSG (10, 30, 60 mg·kg−1) and mesalazine. The mice were administered 10, 30, 60 mg·kg−1 THSG or 100 mg·kg−1 mesalazine or saline once daily by intragastric administration for 7 days after induction of colitis by acetic acid irrigation. THSG dramatically attenuated acetic acid-induced colon lesions, including reversing the body weight loss and improving histopathological changes. THSG apparently decreased the increase of malondialdehyde (MDA) which is a marker of lipid peroxidation. THSG appears to exert its beneficial effects on acetic acid-induced experimental colitis through upregulation of PPAR-γ mRNA and protein levels and inhibition of the NF-κB pathway, which in turn decreases the protein overexpression of the downstream inflammatory mediators TNF-α, IL-6 and COX-2. The effect of THSG 60 mg·kg−1 on PPAR-γ mRNA expression was higher than that of mesalazine. THSG may thus be a promising new candidate or lead compound for the treatment of IBD.
Highlights
Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, have a high incidence in industrialized nations and severely affect the life quality of patients
In this paper we focused on the effects of THSG on PPAR-γ and the NF-κB-induced inflammatory mediators TNF-α, IL-6, COX-2 in an mouse experimental model of colitis induced by acetic acid, with the aim of revealing the underlying mechanisms of the beneficial effects of THSG on colitis and provide evidence that THSG may be a promising new candidate or lead compound for the treatment of IBD
THSG, a polyphenolic compound from Polygonum multiflorum Thunb (PM), had a pretty good effect on experimental colitis induced by acetic acid as judged through the significant reversal of body weight loss and attenuation of histological lesions observed in experimental animals
Summary
Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, have a high incidence in industrialized nations and severely affect the life quality of patients. They are chronic and relapsing inflammatory disorders of the gastrointestinal tract, defined by clinical characteristics such as diarrhea, abdominal pains, weight loss and nausea and by pathological features such as a loss of mucosal integrity and inflammatory cell infiltration [1]. In this paper we focused on the effects of THSG on PPAR-γ and the NF-κB-induced inflammatory mediators TNF-α, IL-6, COX-2 in an mouse experimental model of colitis induced by acetic acid, with the aim of revealing the underlying mechanisms of the beneficial effects of THSG on colitis and provide evidence that THSG may be a promising new candidate or lead compound for the treatment of IBD
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