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首页> 外文期刊>Inflammation >Effects of Trefoil Peptide 3 on Expression of TNF-α, TLR4, and NF-κB in Trinitrobenzene Sulphonic Acid Induced Colitis Mice
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Effects of Trefoil Peptide 3 on Expression of TNF-α, TLR4, and NF-κB in Trinitrobenzene Sulphonic Acid Induced Colitis Mice

机译：三叶肽3对三硝基苯磺酸诱导的结肠炎小鼠TNF-α，TLR4和NF-κB表达的影响

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The trefoil factor (TFF) peptides are major secretory products of mucus cells of the gastrointestinal tract. There were evidences that administration of recombinant human TFF3 is effective in treatment of models of colitis, but the mechanism of the effects of rTFF3 is not fully understood. The main aims of this study is to evaluate effects of intraperitoneal injection recombinant human TFF3 on the expression of tumour necrosis factor α (TNF-α), toll-like receptor 4(TLR4), and nuclear factor κB (NF-κB) in trinitrobenzene sulphonic acid (TNBS) induced colitis mice. Distal colitis was induced in BALB/C mice by intracolonic administration of TNBS in ethanol. Treated with administration rhTFF3 for treatment group(5 mg/ml; approximately 0.5 mg/mouse), and normal saline for control for 5 consecutive days. Colonic damage score, tissue myeloperoxidase (MPO) activity, TLR4, NF-κB mRNA expression, and tissue TNF-α, TLR4, NF-κB production were determined, respectively. Once daily application of hTFF3 for 5 days after TNBS/ethanol had been injected, both microscopic and macroscopic injury and inflammatory index had been reduced compared with controls. In addition, decreased tissue TNF-α, TLR4, NF-κB production, and TLR4, NF-κB mRNA expression had been found. This study has shown that hTFF3 may have therapeutic potential in the treatment of inflammatory bowel disease, and one of the mechanisms may related to inhibit the TLR4/NF-κB signaling pathways.
机译：三叶因子（TFF）肽是胃肠道粘液细胞的主要分泌产物。有证据表明，重组人TFF3的施用可有效治疗结肠炎模型，但尚未完全了解rTFF3的作用机理。这项研究的主要目的是评估腹腔注射重组人TFF3对三硝基苯中肿瘤坏死因子α（TNF-α），toll​​样受体4（TLR4）和核因子κB（NF-κB）表达的影响磺酸（TNBS）诱导的结肠炎小鼠。通过在乙醇中结肠内给药TNBS，在BALB / C小鼠中诱发远端结肠炎。用rhTFF3给药治疗组（5mg / ml；约0.5mg /小鼠），并用生理盐水作对照连续5天治疗。分别测定结肠损伤评分，组织髓过氧化物酶（MPO）活性，TLR4，NF-κBmRNA表达和组织TNF-α，TLR4，NF-κB产生。注射TNBS /乙醇后连续5天每天施用hTFF3，与对照组相比，微观和宏观损伤以及炎症指数均降低。另外，还发现组织TNF-α，TLR4，NF-κB的产生减少，以及TLR4，NF-κBmRNA的表达减少。这项研究表明，hTFF3在炎症性肠病的治疗中可能具有治疗潜力，其机制之一可能与抑制TLR4 /NF-κB信号通路有关。

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