脱氧胆酸促进肠道组织产生IL-1β及诱导肠道炎症作用的研究

发布时间：2018-08-06 08:05

【摘要】：目的:研究高脱氧胆酸(DCA)对肠道促炎因子IL-1β等的表达及肠道炎症的诱导作用。方法:给予小鼠添加DCA的膳食,建立小鼠肠道高DCA模型,采用HE染色观察小鼠肠道病理损伤情况;以Western Blot检测结肠组织成熟IL-1β的产生;以实时PCR检测IL-6、MCP-1的表达水平;通过髓过氧化物酶(MPO)活力检测肠道炎症情况。结果:给予小鼠添加0.2%DCA的膳食3个月后,其结肠长度明显缩短[对照组(8.1±0.5)cm vs DCA组(7.3±0.3)cm,P0.01];代表肠道炎症程度的指标MPO活性显著上升[对照组(1.6±0.4)U·g~(-1)vs DCA组(3.0±0.5)U·g~(-1),P0.01];HE染色可见结肠黏膜破损,黏膜下水肿及炎症细胞浸润。同时DCA膳食可明显诱导结肠组织成熟IL-1β的产生,并导致促炎因子IL-6(对照组1.0±0.1 vs DCA组174.6±45.9,P0.01)及髓系趋化因子MCP-1(对照组1.0±0.1 vs DCA组187.8±26.2,P0.001)的mRNA水平表达显著升高。结论:高水平DCA可诱导肠道炎症发生,激活炎症小体、促进成熟IL-1β产生可能是其重要作用机制之一。
[Abstract]:Aim: to study the effect of high deoxycholic acid (DCA) on the expression of proinflammatory factor IL-1 尾 and the induction of intestinal inflammation. Methods: the model of high DCA in the intestine of mice was established by adding DCA to the diet, the pathological injury of intestine was observed by HE staining, the production of mature IL-1 尾 in colon tissue was detected by Western Blot, the expression of IL-6 and MCP-1 was detected by real-time PCR. The intestinal inflammation was detected by myeloperoxidase (MPO) activity. Results: the colonic length of mice treated with 0.2A diet for 3 months was significantly shortened [(8.1 卤0.5) cm vs DCA group, (7.3 卤0.3) cm ~ (-1) P0.01], and the activity of MPO, which represented the degree of intestinal inflammation, was increased [(1.6 卤0.4) U g ~ (-1) U g ~ (-1) P ~ (-1) P _ (0.01)]. Submucosal edema and inflammatory cell infiltration. At the same time, DCA diet significantly induced the production of mature IL-1 尾 in colon tissue, and increased the mRNA expression of proinflammatory factor IL-6 (control 1.0 卤0.1 vs DCA 174.6 卤45.9 P0.01) and myeloid chemokine MCP-1 (control 1.0 卤0.1 vs DCA 187.8 卤26.2 P 0.001). Conclusion: high level of DCA can induce intestinal inflammation, activate inflammatory corpuscles and promote mature IL-1 尾 production, which may be one of its important mechanisms.
【作者单位】：上海交通大学医学院附属新华医院;上海市儿科医学研究所;
【基金】：上海市自然科学基金资助项目(16ZR1428500)
【分类号】：R574

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