思连康与美沙拉秦对溃疡性结肠炎患者肠黏膜TLR4、NF-资b表达 与肠道菌群的影响

Objective： To study the curative efficacy of siliankang combining with mesalazine in the treatment of ulcerative colitis and effects on the intestinal mucosa toll like receptor （TLR4）, nuclear factor （NF-κb） expressions and intestinal microflora. Methods： 92 patients with ulcerative colitis who were treated from January 2015 to January 2017 in our hospital were selected and divided into the ob- servation group （n=46） and the control group （n=46） according to random number table. The control group was treated with mesalazine, while the observation group was combined with siliankang, they were continuously treated for 6 weeks. The changes of clinical symptom score, Baron endoscopy score, intestinal mucosal TLR4 and NF-κb expressions and intestinal flora before and after treatment as well as the incidence of adverse events were compared between the two groups. Results： After treatment, the clinical symptom score and Baron endoscopic score of both groups were significantly lower than those before treatment （P 〈 0.05）; the bellyache, diarrhea, pus and blood stool and endoscopic Baron score in the observation group were significantly lower than those of the control group （P〈0.05）; the intestinal mucosal TLR4 and NF-κb expressions of both groups were significantly lower than those before treatment （P 〈 0.05）; the intestinal mu- cosal TLR4 and NF-κb expressions in the observation group were significantly lower than those of the control group （P〈0.05）; the num- ber of bacillus bifidus, lactobacilli, microzyme and clostridium of both groups was significantly changed compared with those before treatment （P〈0.05）; the number of bacillus bifidus, and lactobacilli of observation group were significantly higher than those of the con- trol group, the number ofmicrozyme and clostridium were significantly lower than those of the control group（P〈0.05）; there was no ob- vious adverse reaction in the two groups （P〉0.05）. Conclusion： Siliankang combined with mesalaz ulcerative colitis, the underlying mechanismmay be related to the reduction of intestinal mucosal TLR4 and NF-κb expressions and the regulation the intestinal microecological balance. [ABSTRACT FROM AUTHOR]