Background: NF-kappaB regulates a large number of genes involved in the inflammatory response to critical illness, but it is not well known if and how NF-kappaB is activated in the gut following traumatic brain injury (TBI) and what is the role of cytokine-mediated inflammation in the pathogenesis of acute gut mucosal injury.
Materials And Methods: Male Wistar rats were randomly divided into control and TBI groups, each of which was subgrouped at hours 3, 12, 24, and 72 and on day 7. Parietal brain contusion was produced by a free-falling weight on the exposed dura of the right parietal lobe. NF-kappaB binding activity in jejunal tissue was measured using EMSA and the concentrations of TNF-alpha and IL-6 were detected using ELISA.
Results: NF-kappaB binding activity in the jejunum was significantly increased at 3 h following TBI, was maximal at 72 h, and remained elevated by 7 days postinjury. TNF-alpha and IL-6 concentrations were also significantly increased by 3 h postinjury, but peaked at 24 h and remained elevated on Day 7 postinjury.
Conclusions: TBI induced a rapid and persistent up-regulation of NF-kappaB and proinflammatory cytokines in the gut, which may play an important role in the pathogenesis of acute gut mucosal injury mediated by inflammation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jss.2004.08.002 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Progressive systemic inflammation precedes decompensation in compensated cirrhosis.
JHEP Rep
February 2025
Department of Gastroenterology and Hepatology, Hospital Universitario Ramón y Cajal, Instituto Ramon y Cajal de Investigación Sanitaria (IRYCIS), Universidad de Alcalá, Madrid, Spain.
Background & Aims: Systemic inflammation is a driver of decompensation in cirrhosis with unclear relevance in the compensated stage. We evaluated inflammation and bacterial translocation markers in compensated cirrhosis and their dynamics in relation to the first decompensation.
Methods: This study is nested within the PREDESCI trial, which investigated non-selective beta-blockers for preventing decompensation in compensated cirrhosis and clinically significant portal hypertension (CSPH: hepatic venous pressure gradient ≥10 mmHg).
Modified Gegen Qinlian Decoction Ameliorates DSS-Induced Colitis in Mice via the Modulation of NF-B and Nrf2/HO-1 Pathways.
Mediators Inflamm
January 2025
Institute of Digestive Diseases, Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing, China.
This study aims to reveal the potential molecular mechanisms of modified Gegen Qinlian decoction (MGQD) in relieving ulcerative colitis (UC). C57BL/6J mice were used to establish experimental colitis via dextran sodium sulfate (DSS). Body weight, disease activity index (DAI), spleen weight, colon length, and histopathologic features were measured to evaluate the therapeutic effects of MGQD on mice with UC.
View Article and Find Full Text PDFGualou Guizhi Granule inhibits microglia-mediated neuroinflammation to protect against neuronal apoptosis and .
Front Immunol
January 2025
Institute of Structural Pharmacology and Traditional Chinese Medicine (TCM) Chemical Biology, Fujian Key Laboratory of Chinese Materia Medica, College of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou, China.
Object: Neuroinflammation mediated by microglia has emerged as a critical factor in ischemic stroke and neuronal damage. Gualou Guizhi Granule (GLGZG) has been shown to suppress inflammation in lipopolysaccharide (LPS)-activated microglia, though the underlying mechanisms and its protective effects against neuronal apoptosis remain unclear. This study aims to investigate how GLGZG regulates the Notch signaling pathway in microglia to reduce neuroinflammation and protect neurons from apoptosis.
View Article and Find Full Text PDFExploring the alleviating effects of metabolite lactic acid on non-alcoholic steatohepatitis through the gut-liver axis.
Front Microbiol
January 2025
Department of Infectious Disease, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Objective: This study investigates the protective effects of lactic acid, a metabolite of , on non-alcoholic fatty liver disease (NAFLD) induced by a high-sugar, high-fat diet (HFD) in mice, in the context of the gut-liver axis.
Methods: A NAFLD mouse model was established using a HFD, and different intervention groups were set up to study the protective effects of and its metabolite lactic acid. The groups included a control group, NAFLD group, treatment group, Glyceraldehyde-3-P (G-3P) co-treatment group, and NOD-like receptor family pyrin domain containing 3 (NLRP3) overexpression group.
Curcumin exerts protective effects against valproic acid-induced testicular damage through modulating the JAK1/STAT-3/IL-6 signaling pathway in rats.
Iran J Basic Med Sci
January 2025
Department of Animal Nutrition and Nutritional Disorders, Faculty of Veterinary Medicine, Ataturk University, Erzurum 25240, Turkey.
Objectives: This experiment was carried out to investigate the protective effects of curcumin (CUR) on testicular damage induced by the valproic acid (VPA) administration.
Materials And Methods: Male Wistar-Albino rats (n=28, 250-300 g) were randomly divided into four groups: Control (1 ml saline, oral), VPA (500 mg/kg, IP), CUR (200 mg/kg, oral), or VPA+CUR (500 mg/kg, VPA, IP plus 200 mg/kg CUR, oral). The treatments were applied for 14 days.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!