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作 者:李博林[1] 赵丹阳[1] 杜朋丽 才艳茹 何芳[1] 景璇[1] 杨倩[1] 胡婧楠[1] 李刚[1] LI Bo-Lin;ZHAO Dan-Yang;DU Peng-Li;CAI Yan-Ru;HE Fang;JING Xuan;YANG Qian;HU Jing-Nan;LI Gang(Hebei Provincial Hospital of Traditional Chinese Medicine, Shijiazhuang 050011 Hebei,China)
机构地区:[1]河北省中医院
出 处:《广州中医药大学学报》2019年第7期1045-1049,共5页Journal of Guangzhou University of Traditional Chinese Medicine
基 金:河北省重点研发计划自筹项目(编号:182777163);河北省中医药管理局科研计划项目(编号:2018039)
摘 要:【目的】观察化浊解毒方对溃疡性结肠炎(UC)大鼠结肠受损黏膜的修复作用,并探讨其机制。【方法】将60只雄性Wistar大鼠随机分为正常组15只和造模组45只,采用2,4,6-三硝基苯磺酸(TNBS)/乙醇法诱导UC大鼠模型。造模成功后,将造模组所剩42只大鼠随机分为UC模型组、美沙拉嗪组、化浊解毒方组,每组14只,予相应药物灌胃,1次/d,连续灌胃14 d。观察各组大鼠疾病活动指数(DAI)评分,结肠黏膜组织病理学,血清白细胞介素(IL)-1β、IL-8含量及结肠黏膜核因子kappaB(NF-κB)mRNA表达变化情况。【结果】与UC模型组比较,美沙拉嗪组、化浊解毒方组DAI评分,血清IL-1β、IL-8含量及结肠黏膜NF-κB mRNA表达水平均降低(P<0.05),受损的结肠黏膜组织明显改善;与美沙拉嗪组比较,化浊解毒方组对上述指标的作用效果更明显(P<0.05)。【结论】化浊解毒方可修复UC大鼠结肠受损黏膜,其机制可能与其下调结肠黏膜NF-κB mRNA表达,降低血清促炎因子IL-1β、IL-8含量有关。Objective To observe the repairing effects of Turbidity-resolving and Toxin-removing Recipe(TTR)on the damaged colonic mucosa in rats with ulcerative colitis(UC),and to explore its mechanism. Methods Sixty male Wistar rats were randomly divided into normal group(N = 15)and modeling group(N = 45). The rats in the modeling group were induced into ulcerative colitis by TNBS/ethanol method. After modeling,the remaining 30 successful modeling rats were randomly divided into UC model group,mesalazine group and TTR group,14 rats in each group, and then were give intragatric administration of corresponding drug, the treatment lasting 14 continuous days. The changes of disease activity index(DAI),colonic histopathology,serum contents of IL-1β and IL-8,and colonic mucosal expression level of nuclear factor kappa B(NF-κB)mRNA in various groups were observed. Results Compared with the UC model group,the DAI score,the serum levels of IL-1β and IL-8,and colonic mucosal expression level of NF-κB mRNA in the mesalazine group and TTR group were all decreased(P <0.05),and the damaged colonic mucosal tissues were improved. Compared with the mesalazine group,the effect of the above indexes were significantly obvious in TTR group(P < 0.05). Conclusion TTR is effective for repairing the damaged colonic mucosa of UC rats,and its mechanism may be related with down-regulating the expression level of NF-κB mRNA in colonic mucosa and reducing the serum content of pro-inflammatory factors IL-1β and IL-8.
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