Objective：To investigate whether the α7 nicotinic acetylcholine receptors agonist GTS-21 can ameliorate dextran sulfate sodium(DSS)-induced colitis and its potential mechanism. Methods：Male BALB/c mice(8-10 weeks old) were randomly divided into 3 groups，including the control group，the DSS-induced group，and the GTS-21 treatment group(n=8，each group). DSS model was performed with 3.5% DSS free drink，the GTS-21 treatment group was performed with 3.5% DSS free drink+GTS-21 10 mg/(kg·d)，ip，for 7 d. The control group was given normal saline，and DAI score was given to each group for every day. At day 8，all mice were sacrificed，the changes of the colonic mucosa were observed，the length and wet weight were measured，and the histological inflammation(HI) score was assessed by HE staining. The levels of cytokines were detected by ELISA. Results：①Compared with the control mice，DAI score was increased［(1.51±0.10)vs.0，n=8，P＜0.001］，colon length was shortened［(8.22±0.37)cm vs.(11.65±0.30)cm，n=8，P＜0.001］ and HI score was increased［(20.5±3.9)vs.(0.9±0.4)，n=8，P＜0.001］in mice-induced DSS，which showed that the model was successfully established.②Compared with DSS-induced mice，DAI score was decreased［(0.25±0.10)vs.(1.51±0.10)，n=8，P＜0.001］，shortened colon length was improved［(9.42±0.32)cm vs.(8.22±0.37)cm，n=8，P＜0.05］ and HI score was decreased［(7.5±2.0)vs.(20.5± 3.9)，n=8，P＜0.01］ in mice with administration of GTS-21，which suggested that GTS-21 improved DSS-induced colitis in mice.③The level of CXCL9/Mig in DSS-induced mice was increased，while it was significantly decreased in mice with administration of GTS-21. In addition，tumor necrosis factor α(TNF-α)，interleukin 1β(IL-1β) and interferon γ(IFN-γ) were significantly increased. ④CXCL9/Mig with the most obvious change detected by further ELISA showed that serum CXCL9/Mig increased significantly in the DSS group(P＜0.05)，and after administration of GTS-21，serum CXCL9/Mig was decreased(P＜0.05). Conclusion：α7nAChR agonist GTS-21 can attenuate the intestinal inflammation in DSS-induced mice，which may be due to reduction of CXCL9/Mig(a chemotactic factor)，and then reduction of inflammatory cell aggregation.