论文部分内容阅读
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 therapeutic mechanism of Jiechang Kangtai I on acute inflammation in mice. Methods Female BALB/C mice were randomly divided into normal control group, model group, sulfasalazine (SASP) group and Jiechang Kangtai I group. Except the normal control group, each group was intragastrically administered by DSS after modeling. After administration, the colon tissue of mice was taken for immunohistochemistry and in situ hybridization to observe the expression of NF-κB P65, COX-2 and their mRNA. Results The expression of COX-2, NF-κB P65 and its mRNA in the colon of the model group was significantly higher than that of the normal control group. The expression of COX-2, NF-κB P65 and its mRNA in colon of Kangtai I group was lower than that of the model group. Conclusion Jiechang Kangtai I can reduce the expression of NF-κB P65 and COX-2 in colon tissue of mice with colitis, which may be one of the mechanisms of its efficacy.