| Summary: | 碩士 === 長庚大學 === 中醫學系傳統中醫學 === 104 === Inflammatory bowel disease (IBD) mainly comprised of ulcerative colitis and Crohn's disease are chronic relapsing disorders of the gastrointestinal tract. It has been postulated that alterations in the epithelial barrier function and the inflammatory cytokines infiltration by immune cells from the periphery and the lamina propria could lead to IBD; however, the involved mechanisms are sparse. Ger-Gen-Chyn- Lian-Tang (GGCLT) is a traditional extract mixture of four Chinese medicine herbs, consisting of Puerariae Radix, Coptids Rhizoma, Scutellariae Radix, and Glycyrrhizae Radix and it was commonly used to control inflammatory response and cure acute colitis. Therefore, the aims of present study were firstly to investigate whether GGCLT ameliorates ulcerative colitis induced by dextran sulfate sodium (DSS) in mice. Secondly, to clear the related mechanisms which were participated in inflammation and epithelial injury to confer the modulation of GGCLT on murine colitis.
Male C57BL/6 mice were orally administered with 4% DSS (dissolved in drinking water) or drinking water for 12 days. Subsequently, all mice after receiving DSS developed colitis were randomly divided into 3 subgroups to treat with once daily oral administration of dH2O, 30 and 100 mg/kg body weight of (water extracted) GGCLT at the 4th day of DSS challenge until the experiment was completed. The disease severity, inflammatory responses and mucus layer regeneration of the colon tissue in colitis mice were examined. The results showed that comparing to DSS group, GGCLT potently ameliorated DSS-induced presence of gross blood per rectum, colon shorting and colon histological injury. Further, the infiltration of neutrophils and macrophages as well as the up-regulation in colonic TLR4/MyD88 signaling, NF-κB and PAI-1 levels caused by DSS were reversed in animals treated with the combination therapy of GGCLT. Moreover, GGCLT treatment was pronouncedly increased mucus layer level of Bcl-xL (anti-apoptotic property), Ki-67 (cell proliferation), Cyclin D1 (cycle cycle), Claudin-1 and ZO-1 (tight junction protein) which was suppressed by DSS. Our findings suggested that GGCLT has the potential to improve DSS-induced colitis by inhibiting the inflammatory responses and enhancing the epithelial barrier function through inhibition of TLR4/MyD88 signaling pathway.
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