摘要
【目的】观察溃结灵对溃疡性结肠炎(UC)模型大鼠结肠黏膜细胞间粘附分子-1(ICAM-1)基因表达的作用。【方法】取SD大鼠48只,随机分成正常组,模型组,溃结灵低、中、高剂量组(剂量分别为4.6、9.2、18.3 g/kg),柳氮磺胺吡啶组(SASP组,剂量为0.5 g/kg);采用三硝基苯磺酸(TNBS)法复制UC大鼠模型,3 d后各组按设计剂量连续灌胃给药10 d,正常组及模型组给予等容积蒸馏水;取各组大鼠结肠黏膜组织,采用逆转录—聚合酶链反应(RT-PCR)法检测ICAM-1基因表达水平。【结果】模型组ICAM-1表达水平显著高于正常组(P<0.01);溃结灵中、高剂量组ICAM-1表达水平显著低于模型组(P<0.05或P<0.01),作用与SASP组相仿(P>0.05)。【结论】溃结灵治疗溃疡性结肠炎的作用可能与其能抑制UC模型大鼠结肠黏膜ICAM-1基因表达有关。
Objective Gene expression of intercellular adhesion molecules （ICAM-1） in colonic mucosa of ulcerative colitis （UC） rats was observed to study the therapeutic mechanism of Kuijieling Decoction （KD）. Methods UC rat models were induced by trinitrobenzenesulphonic acid （TNBS）. The rats were randomly divided into six groups： normal control （NC） group, model control （MC） group , low-dose Kuijieling group, middle-dose Kuijieling group, high-dose Kuijieling group and salicylazosulfapyridine （SASP） group. After treatment for 10 days, the rats were killed to get their colonic mucosa. Total RNA was isolated from colonic mucosa by Trizol. With β-actin as internal index, reverse transcription polymerase chain reaction （RT-PCR） was used to detect ICAM-1 expressions. Results Gene expression level of ICAM-1 in MC group was significantly higher than that in NC group （P 〈 0.01 ）. Gene expression level of ICAM-1 in middle- and high-dose KD groups was significantly lower than that in MC group （ P 〈 0. 05 or P 〈 0. 01 ）, but was similar to that in SASP group （ P 〉 0. 05 ）. Conclusion KD has an inhibitory effect on gene expression of ICAM-1 in colonic mucosa of UC model rats induced by TNBS, which may be one of its anti-UC mechanisms.
出处
《广州中医药大学学报》
CAS
2008年第3期229-232,共4页
Journal of Guangzhou University of Traditional Chinese Medicine
基金
国家自然科学基金(编号:30400613)
关键词
溃结灵/药理学
结肠炎
溃疡性/中药疗法
基因表达调控
疾病模型
动物
大鼠
KUIJIELING DECOCTION/pharmacology
COLITIS, ULCERATIVE/TCD therapy
GENE EXPRESSION REGULATION
DISEASE MODELS, ANIMAL
RATS
