Abstract
Kupffer cells play a major role in alcoholic liver disease. Oxidative stress and endotoxin are major mediators of the inflammatory process in alcoholic hepatitis. Recent evidence supports the suggestion that endotoxin-induced signal transduction begins with CD14-mediated activation of Toll-receptor 4 and subsequent activation of nuclear factor-kappa B (NF-κB) binding activity. Free radicals from reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in Kupffer cells also activate NF-κB binding activity. Inflammatory cytokines and cyclooxygenase-2 are up-regulated in response to binding of NF-κB. A combined role for tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 is important in the pathogenesis of alcoholic hepatitis.
| Original language | English |
|---|---|
| Pages (from-to) | 13-15 |
| Number of pages | 3 |
| Journal | Alcohol |
| Volume | 27 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2002 |
| Externally published | Yes |
Bibliographical note
Funding Information:Support was provided by grants from the Alcohol Beverages Medical Research Foundation and the National Institutes of Health.
ASJC Scopus Subject Areas
- Health(social science)
- Biochemistry
- Toxicology
- Neurology
- Behavioral Neuroscience
