In this research, we studied the protective action of the effective fraction isolated from Radix Astragali (EF-RA) against inflammation as well as mucosal and epithelial injury in a murine ulcerative colitis model, and its underlying mechanism by investigating possible involvement of nuclear factorκ-light-chain-enhancer of activated B cells (NF-κ B) and mitogen-activated protein kinase (MAPK) pathways.We hypothesize that EF-RA elicits anti-inflammation and epithelial repairing effects via inhibiting MAPK signaling and interfering with the nuclear translocation of NF-κ B, subsequently resulting in NF-κ B dependent transcriptional repression of inflammatory factors and epithelial cell apoptosis.Mice were exposed to 5 days of dextran sulfate sodium (DSS) in the drinking water;clinical symptoms and histological scoring were evaluated by hematoxylin and eosin (H&E) and immunohistochemistry staining; the expression of pro-inflammatory and anti-inflammatory factors were quantified by enzyme-linked immunosorbent assay (ELISA); the epithelial and mucosal repair action of EF-RA were examined by proliferation, migration and apoptosis assay, intestinal permeability assay, and quantitative analysis of mucus thickness and mucin gene expression.The possible involvement of NFκ B and MAPK pathways were examined by studying the influence of MAPK phosphorylation inhibitors on Young adult murine colon (YAMC) cell apoptosis, secretion of pro-inflammatory factors and NF-κ B nuclear translocation.In acute colitis model, results showed the EF-RA at the doses of 1g/kg and 3g/kg caused death of DSS mice, so that 4 of the 5 mice dead in each group.The body weight and colon length of mice received EF-RA2g/kg didn t show significant difference with DSS group, indicating that EF-RA could not alleviate DSS-caused loss of body weight and colon length.In chronic colitis model, results showed that the colon length, colon MPO content and fecal occult score of EF-RA groups didn t show significant difference with DSS group.However, EF-RA down-regulated the levels of IFN-γ and IL-6.Statistical difference was observed in the EF-RA 0.5g/kg(for IFN-γ).In addition, EF-RA at the dose of 1g/kg significantly increased the expression of IL-10.These results suggest EF-RA could not protect mice from DSS colitis, but did affect the pro-inflammatory and anti-inflammatory cytokines.