Related Experiment Video
Updated: Jan 4, 2026

Murine Model of Intestinal Ischemia-reperfusion Injury
Published on: May 11, 2016
Intestinal mucosal injury induced by obstructive jaundice is associated with activation of TLR4/TRAF6/NF-κB pathways
Xiaopeng Tian1,2, Huimin Zhao2, Zixuan Zhang1
1Medical School of Chinese PLA, Beijing, China.
Objectives:
To investigate the role of TLR4/TRAF6/NF-κB pathways in intestinal mucosal injury induced by obstructive jaundice (OJ).
Methods:
A total of 100 male C57BL/6J mice were randomly assigned to two groups: (I) sham operation (SH); (II) OJ. The mice were sacrificed before operation and on the 1st, 3rd, 5th and 7th day after operation. The blood and terminal ileum were simultaneously collected under the aseptic condition for further detection.
Results:
In the SH group, TLR4 protein and mRNA rarely expressed in the intestinal mucosa of the mice and there were no significant differences at different time points (p>0.05). By contrast, in the OJ group TLR4 protein (0.12±0.06, 0.16±0.08, 0.27±0.10, 0.35±0.12 and 0.41±0.13, respectively) and mRNA (0.49±0.19, 0.62±0.23, 0.98±0.32, 1.42±0.41 and 1.72±0.49, respectively) increased gradually with the extension of time (p<0.05). Also in the OJ group, the levels of DAO and endotoxin in plasma as well as the expressions of NF-κB and caspase-3 increased gradually with the extension of time, showing positive correlation with the expression of TLR4 (p<0.05).
Conclusions:
The expression of TLR4 was significantly up-regulated in the distal ileum of mice with OJ. Activation of the TLR4/TRAF6/NF-κB pathways was involved in the occurrence and development of intestinal mucosal injury and endotoxemia in mice with OJ.
More Related Videos
10:21Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
Published on: September 12, 2019
08:37Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
Published on: April 21, 2015
Related Concept Videos
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Inflammatory Bowel Disease I: Ulcerative Colitis
Inflammatory bowel disease, or IBD, encompasses a group of disorders characterized by chronic inflammation or ulceration of the gastrointestinal tract.
Risk Factors
The exact cause of IBD remains unclear, although it is believed to be due to a mix of genetic, environmental, microbial, and immune factors. Genetic factors are significant in determining susceptibility to IBD, with family history being a critical risk factor. Individuals with a first-degree relative who has IBD are at...
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
Role Of Notch Signalling In Intestinal Stem Cell Renewal
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...