相关实验视频

Updated: Jan 8, 2026

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

Published on: September 12, 2019

TNIP3通过抑制巨细胞中的TAB1/NF-κB/NLRP3信号通路来减轻结肠炎

Shijun Li¹, Jiasheng Liu¹, Hui Zhou¹

¹Department of Gastrointestinal Surgery, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuchang District, Wuhan, 430060, Hubei Province, China.

Digestive diseases and sciences

|December 23, 2025

概括

TNIP3 (TNFAIP3相互作用蛋白3) 通过控制巨细胞两极分化和改善肠道屏障功能,减少炎症性肠病 (IBD) 的炎症. 这表明TNIP3是IBD的潜在治疗点.

科学领域:

胃肠病学胃肠病学
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

炎症性肠道疾病 (IBD) 涉及慢性肠道炎症.
了解巨分化和上皮屏障功能的机制对于IBD治疗至关重要.

研究的目的:

研究TNIP3 (TNFAIP3相互作用蛋白3) 在IBD中调节巨细胞极化和肠上皮质屏障功能的作用.
阐明TNIP3在IBD中的治疗潜力.

主要方法:

利用LPS诱导的RAW 264.7细胞和DSS诱导的小鼠模型用于IBD研究.
通过流动细胞计,ELISA和西式涂抹来评估巨细胞极化.
使用TEER和FITC-dextran透性试验评估了肠上皮屏障功能,并分析了NF-κB激活.

主要成果:

过度表达TNIP3抑制了M1巨细胞的两极分化,并抑制了NF-κB和NLRP3炎症酶激活.
在培养系统中,TNIP3增强了肠上皮质屏障功能,并减轻了DSS引起的肠损伤.
在IBD模型中,TAB1过度表达逆转了TNIP3的保护作用.

结论:

通过TAB1/NF-κB/NLRP3通路抑制M1巨细胞极化,TNIP3减弱了炎症反应.
TNIP3增强了肠上皮质屏障功能,表明其作为IBD治疗点的潜力.

关键词:

炎症性肠道疾病肠道疾病肠道上皮质屏障肠道上皮质屏障巨细胞的两极分化在NF-κB/NLRP3信号通路中.在TNIP3中,TNIP3是TNIP3.

更多相关视频

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice

Published on: April 21, 2015

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Induction of Intestinal Inflammation by Adoptive Transfer of CBir1 TCR Transgenic CD4+ T Cells to Immunodeficient Mice

Published on: December 16, 2021

相关概念视频

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...