摘要
目的探讨结肠康泰Ⅱ号防治结肠炎小鼠肠纤维化的分子机制。方法雌性BALB/C小鼠随机分为正常对照、模型、SASP、结肠康泰Ⅱ组;除正常对照组外,以DSS诱导小鼠产生慢性UC模型后,药物组分别灌胃给药,疗程结束后取小鼠结肠组织免疫组化、原位杂交方法观察TGF-β1、EGF及其mRNA的表达。结果模型组结肠组织TGF-β1及其mRNA的表达均明显高于正常对照组,结肠康泰Ⅱ号组结肠组织TGF-β1及其mRNA的表达低于模型组(均为P<0.05);模型组结肠组织EGF及其mRNA的表达与正常对照组比较无明显差别(均为P>0.05),结肠康泰Ⅱ号组结肠组织EGF及其mRNA的表达均高于模型组(均为P<0.05)。结论降低TGF-β1,增强EGF及其mRNA的表达分别为结肠康泰Ⅱ号防治结肠炎的作用机制。
Objective: To explore the mechanism of jiechangkangtai II on preventing and treating fibrosis in colon tissue of colitis mice. Methods: 100 female BALB/C mice were randomly divided into four groups, normal control, pathological, solfasalazine(SASP) and jiechangkangtai II groups, chronic colitis in mice were induced by dextran sulfate sodium(DSS) except normal control groups. Expression both TGF-β_1, EGF and their mRNA in colon tissue of colitis mice after treatment were tested by immunohistochemistry and hybridization in situ.Results: Expression of TGF-β_1 and mRNA in pathological group were obviously higher than those in normal control group, expression of TGF-β_1 and mRNA in jiechangkangtai II group were lower than those in pathological group (P<0.05);Compared with normal control group, distinction in expression of EGF and mRNA in pathological group were not evident(P>0.05), but expression of EGF and mRNA in jiechangkangtai II group were higher than those in pathological group(P<0.05). Conclusion: To decrease expression of TGF-β_1 and increase expression of EGF were one of pharmacological mechanisms of jiechangkangtai II to prevent fibrosis of colon tissue of colitis.
出处
《中国中医药科技》
CAS
2006年第2期75-77,共3页
Chinese Journal of Traditional Medical Science and Technology
基金
深圳市科技局2004年资助项目No.200405100
