摘要
目的探寻结肠康泰Ⅰ号对小鼠结肠急性炎症的疗效机制。方法雌性BALB/C小鼠随机分为正常对照组、模型组、柳氮磺胺吡啶(SASP)组和结肠康泰Ⅰ号组;除正常对照组外,以DSS造模后,各药物组分别灌胃给药,疗程结束后取小鼠结肠组织作免疫组化、原位杂交方法观察NF-κBP65、COX-2及其mRNA表达。结果模型组结肠组织COX-2、NF-κBP65及其mRNA表达均明显高于正常对照组,结肠康泰Ⅰ号组结肠组织COX-2、NF-κBP65及其mRNA表达低于模型组。结论结肠康泰Ⅰ号能降低结肠炎小鼠结肠组织NF-κBP65、COX-2的表达,可能是其疗效的机制之一。
Objective:To explore the mechanism of Jiechangkangtai Ⅰ (结 肠 康 泰 1号 ) on curative effect in acute colitis mice.Methods:Balb/c female mice were randomly divided into the normal controlled group,the thepathological group,the solfasalazine(SASP) group,and the Jiechangkangtai Ⅰ group.The pathlolgical model of acute colitis was induced by feeding with DSS in mice,the SASP group and the Jiechangkangtai Ⅰ group mice were fed SASP,Jiechangkangtai Ⅰ respectively,the expression both NF- κ BP65,COX- 2 and the mRNA in colon tissue of acute colitis mice after treatment were examined by immunohistochemistry and hybridization in situ.Results:The expression of NF- κ BP65,COX- 2 and the mRNA in colon tissue in the thepathological group were higher than those in the normal controlled group;the expression of NF- κ BP65,COX- 2 and the mRNA in the Jiechangkangtai Ⅰ group were lower than those in the thepathological group.Conclusion:Jiechangkangtai Ⅰ could decrease the expression NF- κ BP65,COX- 2 in colon tissue of acute colitis mice,that may be one of cutative mechanisms of the drug.
出处
《中国中医急症》
2006年第4期403-405,共3页
Journal of Emergency in Traditional Chinese Medicine
