Anti-inflammatory Effects of Lycium barbarum Polysaccharides and/or Bifidobacterium longum in Rats With DSS-Induced Ulcerative Colitis

Objectives: This study investigated the protective effects of Lycium barbarum polysaccharides (LBP) and/or Bifidobacterium longum OLP-01 (OLP-01) on colonic inflammation in rats with dextran sulfate sodium (DSS)-induced ulcerative colitis (UC). Methods: Male Sprague-Dawley rats aged 7-week-old were divided into 5 groups: normal (N), DSS-induced UC (U), UC and treated with 100 mg LBP/kg bw (L), UC and treated with 2 × 109 CFU OLP-01/kg bw (B), and UC and treated with both 50 mg LBP/kg bw and 1×109 CFU OLP-01/kg bw (M) groups. Treatments of LBP and OLP-01 were administered orally through gavage for 39 days. From day 29 to day 35, rats were orally administered 5% DSS in drinking water continuously for 7 days to induce UC. The colon was collected for analysis on day 39. Histological analysis for colonic damage was determined by hematoxylin and eosin stain. Colonic pro-inflammatory interleukin 6 (IL-6) levels and cyclooxygenase-2 (COX-2) protein were measured respectively by enzyme-linked immunosorbent assay and western blot. Results: Histological observation showed ulceration of the epithelial layer, loss of normal mucosal architecture, and full-thickness inflammation of the colon wall accompanied by a significant increase in histological disease scores in the DSS-treated group. Rats supplemented with LBP and/or OLP-01 had less colonic damage with significantly lower histological disease scores compared to the DSS-treated group. The DSS-treated group significantly increased colonic IL-6 levels, while all treatment groups significantly decreased colonic IL-6 levels. Colonic COX-2 protein involved in inflammation was significantly increased in the rats with colitis, and was significantly decreased in all the treatment groups compared to that in the DSS-treated group. Conclusions: LBP and/or OLP-01 alleviate colon damage with decreased histological disease scores, and inhibit inflammation via reducing IL-6 secretion and COX-2 protein expression in DSS-induced ulcerative colitis rats. Funding Sources: This research was funded by the National Science and Technology Council, Taiwan.