Effects of Anchang Decoction on TLR 4/NF-κB Signaling Pathway and the Expression of Fecal Calprotectin in Rats with Ulcerative Colitis Induced by TNBS / 中国药房

ABSTRACT

OBJECTIVE：To st udy the effects of Anchang decoction on TLR 4/NF-κB signaling pathway and the expression of fecal calprotectin （FC）in TNBS-induced ulcerative colitis （UC）model rats . METHODS ：SD rats were randomly divided into blank group ，model group ，positive control group [Live Bifidobacterium capsules ，5 mL（containing Bifidobacterium 0.35 g）]， Anchang decoction low -dose，medium-dose and high-dose groups （1，5，10 mL，each milliliter is approximately equivalent to 0.11 g of total crude drug ），with 15 rats in each group. Other groups were given TNBS combined with ethanol enema to establish UC model rat ，except blank group was given normal saline. Two days after successful modeling ，blank group and model group were given normal saline 5 mL，administration groups were given relevant medicine intragastrically ，once a day ，for consecutive 14 d. After last medication ，HE staining was used to observe the pathological change of colon tissue in rats. Western blotting assay was used to detect the protein expression of TLR 4，TRAF6 and NF-κB in colon tissues of rats；Real-time fluorescent quantitative PCR was used to detect mRNA expression of TLR 4，TRAF6，TNF-α and NF-κB；ELISA assay was adopted to detect serum level of TNF-α，IL-6 and FC in stool samples. RESULTS ：Compared with blank group ，the colonic mucosa of model group was severely damaged，and the protein expression of TLR 4，TRAF6 and NF-κB，mRNA expression of TLR 4，TRAF6，TNF-α and NF-κb as well as serum levels of TNF-α，IL-6 and FC level in stool samples were increased significantly （P＜0.05）. Compared with model group，the pathological changes of colon tissue in rats were improved in different administration groups to different extents ，and above indexes were all decreased significantly （P＜0.05）. CONCLUSIONS ：Anchang decoction may relieve the inflammation of UC model rats by regulating the TLR 4/NF-κB signaling pathway and the expression of FC.