摘要
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 proinflammator
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 proinflammator
基金
Supported by Guangdong Administration of Traditional Chinese Medicine(No.201 01 92)
