Abstract
Intercellular adhesion molecule-1 (ICAM-1) is associated with processes of inflammation. We investigated the effects of deoxypodophyllotoxin (DPT) on tumor necrosis factor-α (TNF-α) induced ICAM-1 expression in the mouse lung epithelial cell line, LA4. DPT (5 to 20 nM) inhibited TNF-α-induced ICAM-1 expression through nuclear factor-kappa B (NF-κB) in a dose-dependent manner and repressed ICAM-1 promoter activity. NF-κB reporter gene activity and DNA binding activity were also strongly inhibited. In addition, DPT inhibited degradation by the TNF-α induced inhibitory kB-α (IκB-α) in a concentration-dependent manner. Taken together with our previous results suggest DPT might provide a basis for novel anti-inflammatory drug development.
| Original language | English |
|---|---|
| Pages (from-to) | 1-5 |
| Number of pages | 5 |
| Journal | Biological and Pharmaceutical Bulletin |
| Volume | 33 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 2010 |
Keywords
- Deoxypodophyllotoxin
- Intercellular adhesion molecule-1
- Lipopolysaccharide
- Nuclear factor-kappa B
- Tumor necrosis factor-α