Background: The cause of ulcerative colitis (UC) is not known, which maybe involve genetics, environment, immunity and other factors. Most conventional forms of drug therapy suppress or modify the host immunoinflammatory response and neglect the other contributor to disease pathogenesis-the environmental microflora. In recent years, growing evidence exists for a role of the intestinal microflora in the pathogenesis of UC. Therefore, treatment with probiotics has been proposed. Probiotics are viable non-pathogenic microorganisms that confer health benefits to the host by improving the microbial balance of the indigenous microflora.Objective: To evaluate the clinical efficacy of bifico combined with mesalazine in patients with mild-to-moderate active UC, and to explore its mechanism.Method: In total, sixty patients with mild-to-moderate active UC were recruited and were randomised to combination group (n=30) and mesalazine group (n=30). The patients in combination group was treated by bifico(420mg three times daily) and mesalazine(1000 mg four times daily), and only by mesalazine (1000 mg four times daily) in mesalazine group. The study lasted for eight weeks and patients were assessed by clinical symptoms and endoscopic activity indices (Rachmilewitz) as well as drug adverse reaction before and after the treatment. The expression of NF-κB, TNF-αand COX-2 in colonic mucosa was also studied by immunohistochemical staining.Results: The clinical symptoms and endoscopic activity indices (Rachmilewitz) were improved more in combination group than in mesalazine group (P<0.05). The expression of NF-κB, TNF-αand COX-2 significantly decreased in combination group than that in mesalazine group (P<0.05). Safety profile and tolerability were very good for both groups and were not different (P>0.05).Conclusion: The combination of bifico and mesalazine is more effective than mesalazine alone in treatment of mild-to-moderate active UC. Bifico is an effective and safe agent in the treatment of mild-to-moderate active UC probably by inhibiting activity of NF-κB and decreasing expression of TNF-αand COX-2. |