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IBS-D大鼠结肠TLR4、NF-κB的表达变化及机制
作者:鲍璐璐 崔立红 
单位:100048  北京 安徽医科大学海军临床学院(鲍璐璐) 100048  北京 解放军总医院第六医学中心消化内科(鲍璐璐、崔立红) 
关键词:肠易激综合征 腹泻型 大鼠 炎性因子 
分类号:R574
出版年,卷(期):页码:2019,44(8):648-651
摘要:

[摘要]  目的  探讨腹泻型肠易激综合征(IBS-D)大鼠结肠Toll样受体4(TLR4)、核因子κB(NF-κB)的表达变化及机制。方法  利用急慢性应激法构建IBS-D大鼠模型,并随机分为空白组(除急慢性应激处理外不做其他处理)IBS-D(在急慢性应激处理前给予3mg/kg生理盐水)TAK-242(急慢性应激处理同期给予3mg/kg TAK-242),每组10只。建模后07142128d观察大鼠饮食、饮水、精神状态、毛色变化、大便性状等一般情况。采用Bristol分型评价粪便性状,评价造模是否成功。收集建模后各时间点大鼠尾静脉血,采用ELISA法检测血清MyD88IL-1βIL-6水平;取造模后28d大鼠结肠组织,采用Western blotting检测TLR4NF-κB的表达水平。结果  造模后7142128d,空白组大鼠Bristol大便分型积分及MyD88IL-1βIL-6TLR4NF-κB水平均无明显变化;造模后7142128dIBS-D组和TAK-242组大鼠Bristol大便分型积分,血清MyD88IL-1βIL-6水平,以及结肠组织TLR4NF-κB表达水平均明显高于空白组(P0.05),且IBS-D组明显高于TAK-242(P0.05)结论  IBS-D可能通过TLR4/MyD88/NF-κB导致炎性因子的产生,进而促进IBS-D的发生发展。

[Abstract]  Objective  To analyze the dynamic changes of inflammatory factors in rats model induced with IBS-D. Methods  Thirty Wistar rats were randomly divided into the blank group, the IBS-D group, and the TAK-242 group. All rats received acute and chronic stress method, followed by no further treatment for the blank group. To induce IBS-D, before performing acute and chronic stress, the IBS-D group received 3 mg/kg saline. To explore the potential mechanism of TLR4 in IBS-D, TAK-242, an antagonist of TLR4 was given to 3 mg/kg TAK-242 group after they received acute and chronic stress. Fecal traits were evaluated by Bristol classification at 0, 7, 14, 21, 28 days, and the levels of MyD88, IL-1β, IL-6 were quantified by Elisa assays; and the levels of TLR4, NF-κB were detected by Western blot. Results  In the blank group, there was no significant change in the scores of Bristol stool and expression levels of MyD88, IL-1β, IL-6, TLR4 and NF-κB at the 7th, 14th, 21st and 28th day. Compared with the blank group, in the IBS-D rats and TAK-242 rats, the scores of Bristolian stools (P<0.05), the levels of MyD88 and serum inflammatory factors (P<0.05), TLR4, NF-κB were all increased (P<0.05). However, the scores of Bristolian stools and the expression levels of MyD88, IL-1β, IL-6, TLR4, and NF-κB in the TAK-242 group were lower than those in the IBS-D group, suggesting therapeutic effects of TAK-242 in IBS-D. Conclusions  IBS-D may increase inflammatory factors through activating the TLR4/MyD88/NF-κB signaling pathway, resulting in disease progression.

基金项目:
国家自然科学基金面上项目(81670494)
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