Effects of Trefoil Peptide 3 on Expression of TNF-α, TLR4, and NF-κB in Trinitrobenzene Sulphonic Acid Induced Colitis Mice

被引:45
作者
Teng, Xu [1 ]
Xu, Ling-Fen [1 ]
Zhou, Ping [1 ,2 ]
Sun, Hong-Wei [1 ]
Sun, Mei [1 ]
机构
[1] China Med Univ, Dept Pediat Gastroenterol, Shengjing Hosp, Shenyang 110004, Liaoning, Peoples R China
[2] Harbin Med Univ, Dept Pediat, Affiliated Hosp 2, Harbin 150086, Heilongjiang, Peoples R China
关键词
trefoil peptide; TFF3; colitis; immune regulation; TLR4/NF-kappa B; TOLL-LIKE RECEPTORS; INFLAMMATORY-BOWEL-DISEASE; CROHNS-DISEASE; ULCERATIVE-COLITIS; INNATE; TFF2; IDENTIFICATION; RESISTANCE; INFLIXIMAB; FACTOR-2;
D O I
10.1007/s10753-009-9110-x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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 alpha (TNF-alpha), toll-like receptor 4(TLR4), and nuclear factor kappa B (NF-kappa B) 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-kappa B mRNA expression, and tissue TNF-alpha, TLR4, NF-kappa B 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-alpha, TLR4, NF-kappa B production, and TLR4, NF-kappa B 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-kappa B signaling pathways.
引用
收藏
页码:120 / 129
页数:10
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