Coptisine ameliorates DSS-induced ulcerative colitis via improving intestinal barrier dysfunction and suppressing inflammatory response

Ulcerative colitis (UC), as an autoimmune disease, has been troubling human health for many years. Up to now, the available treatments remain unsatisfactory. Rhizoma Coptidis has been widely applied to treat gastrointestinal diseases in China for a long time, and coptisine (COP) is identified as one of its major active components. This study aimed to evaluate the bioactivity of COP on dextran sulfate sodium (DSS)-induced mice colitis and clarify the potential mechanism of action. The results revealed that COP treatment markedly alleviated DSS-induced clinical symptoms by relieving body weight loss and the disease activity index (DAI) score. Specifically, the colon length in the COP (50 and 100 mg/kg) groups were obviously longer than that in the DSS group (7.21 +/- 0.34, 8.59 +/- 0.45 cm vs. 6.71 +/- 0.59 cm, P < 0.01). HE staining analysis revealed that COP treatment significantly protected the integrity of intestinal barrier and alleviated inflammatory cells infiltration. Western blot assay confirmed that COP notably improved the intestinal epithelial barrier function by enhancing the expressions of colonic tight junction proteins and inhibited the expressions of apoptosis-related proteins. In addition, COP treatment remarkably suppressed the levels of colonic myeloperoxidase (MPO), adhesion molecules and pro-inflammatory cytokines (TNF-alpha, IFN-gamma, IL-1 beta, IL-6 and IL-17), while enhanced IL-10 and TGF-beta. The mechanism anti-inflammatory of COP might be related to inhibiting the phosphorylation of I kappa B alpha, and the translocation of NF-kappa B p65 from cytoplasm to nucleus. In summary, the study indicated that COP ameliorated DSS-induced colitis, at least partly through maintaining the integrity of intestinal epithelial barrier, inhibiting apoptosis and inflammatory response.

Automated summary

Coptisine has demonstrated therapeutic effects on ulcerative colitis by maintaining the integrity of the intestinal epithelial barrier, inhibiting apoptosis, and inflammatory response.