To observe the protective effect of Changyanqing on rats with ulcerative colitis and its regulation of transforming growth factor-β1(TGF-β1)/mothers against decapentaplegic homolog 3(Smad3)/extracellular signal-regulated kinases(ERK) signaling pathway.Methods:A total of 25 female SD rats were randomly divided into 5 groups:blank control group,model group,mesalazine group,Changyanqing low-dose group and Changyanqing high-dose group.Except for the blank control group,the rest rats were injected with 2,4,6-Trinitrobenzenesulfonic acid(TNBS) to establish a UC model.Then 24 h after modeling,the TNBS model group and the blank control group were given 0.9% normal saline by gavage; the mesalazine group was given 30 mg/kg mesalazine suspension by gavage; the Changyanqing high-and low-dose groups were intragastrically administered with 147.2 g/kg and 36.8 g/kg Changyanqing,respectively,at a fixed time once a day for 7 days.The phosphorylation level of TGF-β1,Smad3,and ERK and the activation degree of TGF-β1 signaling pathway in colonic mucosa were detected.Results:The ERK expression level in the model group was the lowest among all groups.The ERK expression level in Changyanqing high-and low-dose groups increased with the increase of the dose,and this index of Changyanqing high-dose group was significantly higher than that of the model group.The levels of TGF-β1 and Smad3 in the model group were the highest among all groups.Conclusion:Changyanqing had a protective effect on the intestinal mucosa of UC rats and played a role in intestinal repair,and its mechanism of action might be related to down-regulating the TGF-β1/Smad3 pathway and increasing the expression of ERK.