雷公藤甲素对炎症性肠病模型小鼠吻合口纤维化及肿瘤坏死因子-α/微小RNA-155轴的影响  

Triptolide attenuate the anastomosis fibrosis of interleukin-10-/-mice performed ileocaecal resection by downregulating tumor necrosis factor-α/microRNA-155 axis

作　　者：吴茸[1] 王栋[1] 张志刚[1] 邵翔宇[1] 陶庆松[1] 李俊生[1] 嵇振岭[1] 

机构地区：[1]东南大学附属中大医院普外科,南京210000

出　　处：《中华实验外科杂志》2015年第9期2182-2184,共3页Chinese Journal of Experimental Surgery

摘　　要：目的 观察雷公藤甲素对行回盲部切除、回肠结肠吻合术后炎症性肠病模型小鼠[白细胞介素（IL）-10基因敲除]吻合口纤维化及肿瘤坏死因子-α（TNF-α）/微小RNA（miR）-155轴的影响.方法 将IL-10基因敲除小鼠行回盲部切除、回肠结肠吻合术建立模型后腹腔注射雷公藤甲素4周后处死,取吻合口附近肠管行天狼猩红染色,并进行组织学评分,Western blot检测前胶原α1的表达,实时定量反转录聚合酶链反应（RT-qPCR）检测miR-155、TNF-α的水平,酶联免疫吸附试验（ELISA）法检测吻合口肠管TNF-α、IL-6、转化生长因子（TGF）-β的含量.结果 经过雷公藤甲素治疗后,IL-10基因敲除小鼠的吻合口纤维化水平较对照组明显下降,吻合口组织内前胶原α1的含量亦明显下降（TT-ICR组0.81 ±0.23、对照组1.47 ±0.47,P＜0.05）.雷公藤组小鼠吻合口内miR-155、TNF-α的水平较对照组明显下降（miR-155：TT-ICR组0.25±0.12、对照组1.00±0.00,P＜0.05;TNF-α：TT-ICR组0.56±0.11、对照组1.00±0.00,P＜0.05）,且与纤维化密切相关的细胞因子IL-6、TGF-β的水平也明显下降.结论 雷公藤甲素可以抑制炎症性肠病模型小鼠吻合口的纤维化过程,这可能与雷公藤甲素抑制了肠道TNF-α/miR-155轴的表达有关.Objective To investigate the influence of triptolide on fibrosis of interleukin （IL）-10 deficient mice anastomosis and tumor necrosis factor-α （TNF-α） /microRNA （miR）-155 axis.Methods 12 interleukin-10 deficient mice which underwent ileocaecal resection were randomized to control and triptolide group.4 weeks after the start of experiment,a 1 cm segment spanning the anastomosis was collected for histology,real-time reverse transcriptase-polymerase chain reaction （RT-qPCR）,Western blotting and enzyme linked immunosorbent assay （ELISA）.Results After the treatment of triptolide,both fibrosis score and the level of procollagen-α1 were decreased（TT-ICR group 0.81 ± 0.23 vs.control group 1.47 ± 0.47,P ＜ 0.05）.The level of miR-155 in triptolide group was decreased （TT-ICR group 0.25 ± 0.12 vs.control group 1.00 ± 0.00,P ＜ 0.05）,as well as the level of TNF-α （TT-ICR group 0.56 ±0.11 vs.control group 1.00 ±0.00,P ＜0.05）,interleukin （IL）-6 and transforming growth factor （TGF）-β.Conclusion Our results suggested that triptolide attenuate the anastomosis fibrosis of IL-10-/-mice performed ICR by the mechanism involving downregulation of TNF-α/miR-155 axis.

关 键 词：雷公藤甲素 炎症性肠病小鼠 克罗恩病 微小RNA-155 纤维化 

分 类 号：R587.1[医药卫生—内分泌]