CAJ | 학술논문

目的通过观察红花注射液(ICT)对2,4,6-三硝基苯磺酸(2,4,6-TNBS)诱导的大鼠溃疡性结肠炎(UC)的疗效及其对结肠黏膜中粘蛋白(MUC2)、白细胞介素6(IL-6)表达的影响,探讨其作用机制.方法将30只健康雄性 Wistar 大鼠随机分为对照组10只、模型组10只与红花组10只.采用 TNBS 灌肠法复制大鼠UC 模型,红花组同时给予 ICT 干预治疗,模型组与对照组给予等量生理盐水.造模10d 后,对大鼠行疾病活动指数(DAI)、结肠大体形态评分及组织学损伤评分,分别用免疫组织化学法及实时荧光定量 PCR(RT-PCR)技术观察大鼠结肠黏膜中 MUC2,IL-6的表达.结果与对照组相比,实验组与模型组 DAI 评分、结肠大体形态评分、组织学损伤评分均升高,而实验组比模型组显著改善(P <0.01);与对照组相比,模型组 MUC2表达显著降低,而红花组又比模型组显著升高(P <0.05).模型组 IL-6表达显著升高,而红花组又比模型组显著降低(P <0.05).结论 ICT 对 UC 大鼠疗效显著,其作用机制之一可能是通过上调结肠黏膜 MUC2及下调 IL-6的表达,增强肠黏膜屏障作用,减轻炎症反应.
목적통과관찰홍화주사액(ICT)대2,4,6-삼초기분광산(2,4,6-TNBS)유도적대서궤양성결장염(UC)적료효급기대결장점막중점단백(MUC2)、백세포개소6(IL-6)표체적영향,탐토기작용궤제.방법장30지건강웅성 Wistar 대서수궤분위대조조10지、모형조10지여홍화조10지.채용 TNBS 관장법복제대서UC 모형,홍화조동시급여 ICT 간예치료,모형조여대조조급여등량생리염수.조모10d 후,대대서행질병활동지수(DAI)、결장대체형태평분급조직학손상평분,분별용면역조직화학법급실시형광정량 PCR(RT-PCR)기술관찰대서결장점막중 MUC2,IL-6적표체.결과여대조조상비,실험조여모형조 DAI 평분、결장대체형태평분、조직학손상평분균승고,이실험조비모형조현저개선(P <0.01);여대조조상비,모형조 MUC2표체현저강저,이홍화조우비모형조현저승고(P <0.05).모형조 IL-6표체현저승고,이홍화조우비모형조현저강저(P <0.05).결론 ICT 대 UC 대서료효현저,기작용궤제지일가능시통과상조결장점막 MUC2급하조 IL-6적표체,증강장점막병장작용,감경염증반응.
@@@@ Objective To investigate the effects of injection of carthamus tinctorius (ICT) on the expression of mucin 2(MUC2) and interleukin-6(IL-6) in the colonic mucosa of rats with ulcerative colitis and to study the function and mechanism of SS in rats with ulcer -ative colitis.Methods Thirty Wistar rats were divided randomly into control group (10),ICT group(10) and TNBS group(10).Ulcerative colitis was induced in the ICT group and TNBS group by rectal administration of trinitrobenzene sulphonic acid (TNBS).At the same time ICT group was treated with ICT.Control group and model group were treated with sodium chloride .After ten days,all rats were killed.Disease ac-tivity index(DAI),mucosal lesion area and histological damage scores were assessed ,and the expression of MUC2 and IL-6 in the colonic mucosa was detected by immunohistochemistry and real -time fluorescent quantification polymerase chain reaction .Results Compared with the model group,the DAI,mucosal lesion area and histological damage scores in ICT group were significantly decreased (P <0.05);Com-pared with model group,the levels of MUC2 in ICT group were significantly increased (P <0.05);the levels of IL-6 in experimental group were significantly decreased(P <0.05).Conclusion ICT can exert protective effects against rat ulcerative colitis perhaps by upregulating MUC2 expression and downregulating IL -6 expression.