Objective:To investigate the effect of total alkaloids of Sophora alopecuroides(TASA) on dextran sulfate sodium(DSS)-induced colitis in mice.Methods:Chronic experimental colitis was induced by administration of 4 cycles of 4%DSS.Fifty mice were randomly distributed into 4 groups(normal,DSS,DSS/high-dose TASA, and DSS/low-dose TASA groups) by a random number table with body weight stratification.Mice in the normal group(n=11) and DSS-induced colitis control group(n=15) received control treatment of 20 mL/kg distilled water; DSS plus TASA high- and low-dose groups(n=12 each) were treated with TASA solution(20 mL/kg) at the doses of 60 mg/kg and 30 mg/kg,respectively.The severity of colitis was assessed on the basis of clinical signs, colon length,and histology scores.Moreover,secretory immunoglobulin A(slgA) and haptoglobin(HP) were analyzed by enzyme linked immunosorbent assay;intercellular adhesion molecule 1(ICAM-1) and macrophage-migration inhibitory factor(MIF) gene expressions were analyzed by quantitative reverse transcriptase realtime polymerase chain reaction(qRT-PCR) using SYBA greenⅠ;and nuclear factorκB(NF-κB) expression and activation and p65 interaction with the promoter of ICAM-1 gene were assessed by Western blotting and chromatin immunoprecipitation assay.Results:TASA administration significantly attenuated the damage and substantially reduced HP elevation and maintained the level of cecum slgA.TASA inhibited the ICAM-1 gene expression and had no effect on MIF gene expression.Also,TASA was able to reduce phospho-lκBα(p-lκBα) protein expression;however,it had no effect on the activation of IκB kinaseα(IKKα) and inhibitor of NF-κBα(IκBα).Moreover,TASA inhibited the p65 recruitment to the ICAM-1 gene promoter.Conclusions:TASA had a protective effect on DSS-induced colitis.Such effect may be associated with its inhibition of NF-κB activation and blockade of NF-κB-regulated transcription activation of proinflammatory mediator gene. Objective: To investigate the effect of total alkaloids of Sophora alopecuroides (TASA) on dextran sulfate sodium (DSS) -induced colitis in mice. Methods: Chronic experimental colitis was induced by administration of 4 cycles of 4% DSS. Fifty mice were randomly distributed into 4 groups (normal, DSS, DSS / high-dose TASA, and DSS / low-dose TASA groups) by a random number table with body weight stratification. Micr in the normal group (n = 11) and DSS- induced colitis control DSS plus TASA high and low-dose groups (n = 12 each) were treated with TASA solution (20 mL / kg) at doses of 60 mg / kg and 30 mg / kg, respectively. The severity of colitis was assessed on the basis of clinical signs, colon length, and histology scores. More than, secretory immunoglobulin A (slgA) and haptoglobin (HP) were analyzed by enzyme linked immunosorbent assay ; intercellular adhesion molecule 1 (ICAM-1) and macrophage-migration inhibitory factor (MIF) gene expressions were analyzed by quantitative reverse transcriptase realtime polymerase chain reaction (qRT-PCR) using SYBA green I; and nuclear factor kB (NF-κB) expression and activation and p65 interaction with the promoter of ICAM-1 gene were assessed by Western blotting and chromatin immunoprecipitation assay. Results: TASA administration significantly attenuated the damage and substantially reduced HP elevation and maintained the level of cecum slgA. TASA inhibited the ICAM-1 gene expression and had no effect on MIF gene expression. Also, TASA was able to reduce phospho-lκBα (p -lκBα) protein expression; however, it had no effect on the activation of IκB kinaseα (IKKα) and inhibitor of NF-κBα (IκBα). Coreover, TASA inhibited the p65 recruitment to the ICAM-1 gene promoter. Conclusions: TASA had a protective effect on DSS-induced colitis. Inhibitory may be associated with its inhibition of NF-κB activation and blockade of NF-κB-regulated transcription activation of proinflammatory mediator gene.