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抑制IL-1β表达对实验性小鼠溃疡性结肠炎的影响
  • 时间:0
  • 分类:R574.62[医药卫生—消化系统;医药卫生—临床医学;医药卫生—内科学]
  • 作者机构:[1]南通大学附属医院感染性疾病科,江苏226001, [2]南通大学附属医院消化科,江苏226001
  • 相关基金:国家自然科学基金项目(81572397); 南通市科技计划项目(BK2012074)
中文摘要:

目的:建立小鼠结肠炎模型,予以抑制白介素-1β(IL-1β)的表达,分析IL-1β与溃疡性结肠炎(UC)发生发展的相关性。方法:建立与人UC相似的葡聚糖硫酸钠(DSS)小鼠结肠炎动物模型,雌性BALB/c小鼠40只分为4组(n=10):正常对照组、DSS模型组、美沙拉嗪治疗组、地塞米松治疗组。正常对照组小鼠自由饮用蒸馏水7天,其余3组小鼠饮用5%DSS溶液7天。从给DSS第3天开始,美沙拉嗪治疗组胃管注入美沙拉嗪20mg·kg^-1,每天3次,共5天;地塞米松治疗组给予地塞米松0.1mg·kg^-1(0.2m L),腹腔注射,每天1次,共5天。ELISA检测血清IL-1β浓度、RT-PCR、Western Blot检测结肠黏膜IL-1β表达变化,观察各组小鼠治疗前后疾病活动指数、结肠病理大体形态评分、组织学病理评分。结果:血清及局部组织检测提示IL-1β在正常对照组中微弱表达,在DSS模型组中表达明显上调,两组比较差异有统计学意义(P〈0.05);地塞米松组、美沙拉嗪组IL-1β表达低于DSS模型组,差异有统计学意义(P〈0.05);地塞米松治疗组、美沙拉嗪治疗组小鼠结肠炎症状明显改善。结论:IL-1β在小鼠UC中表达上调,参与疾病的发生发展,抑制其表达可治疗溃疡性结肠炎。

英文摘要:

Objective:The study was designed to detect the expression of IL-1β by establishing mice colitis model arising from dextran sodium sulphate(DSS) which was similar to ulcerative colitis(UC) of humans, and to give DXM or Mesalazine to interfere with the model so as to discuss whether there was a correlation between the treatment effect and the inhibition of the expression of IL-1β. Methods: A mice colitis model was set up: BALB/C female mice(n=40)were divided into 4 groups: the normal group(n=10), the DSS model group(n=10), the Mesalazine treatment group(n=10), and the DXM treatment group(n=10). The normal group were given distilled water freely for 7 days, and all of them were put to death by luxation vertebrae on the 8th day. The others were given the same solution of 5% DSS to drink for 7 days, and were put to death in the same way on the 8th day. Among them, the DSS model group were given NS(0.2 m L) by intraperitoneal injection every day from the third day to the 7th day; the mesalazine treatment group were given Mesalazine of 20~30mg·kg-1·d-1by injection into the Stomach tube; Dexamethasone treatment group were given dexamethasone of 0.1 mg·kg-1·d-1(0.2 m L) in the same way. The obvious pathological changes in the colon tissue of all groups were taken to detect the expression of IL-1β by ways of RT-PCR and Western Blot. Results:IL-1β was expressed faintly in the normal mice group, and was upregulated in the mice colitis model arising from DSS. The normal group had statistically significant difference from the DSS model group(P〈0.05). The levels of IL-1β in the Mesalazine treatment group and Dexamethasone treatment group were lower than in the DSS model group(P〈0.05). Conclusions:The expression of IL-1β was up-regulated in the mice models of UC arising from DSS, and was closely related with the occurrence and development of UC. Therefore, inhibition of IL-1βexpression by TL might be a useful treatment method for UC.

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