Effects of thalidomide and related metabolites in a mouse corneal model of neovascularization.
Exp Eye Res
; 64(6): 971-8, 1997 Jun.
Article
em En
| MEDLINE
| ID: mdl-9301478
ABSTRACT
Thalidomide, when administered orally, is an inhibitor of angiogenesis in the basic fibroblast growth factor (bFGF)-induced rabbit cornea micropocket assay. We now show in the mouse that thalidomide given intraperitoneally but not orally significantly inhibits bFGF-induced and vascular endothelial growth factor (VEGF)-induced corneal neovascularization. We further demonstrate that this inhibition is independent from thalidomide's ability to suppress tumor necrosis factor-alpha (TNF-alpha) production. Experiments examining thalidomide's enantiomers reveal-that the S(-)-enantiomer has the strongest antiangiogenic activity in VEGF-induced and bFGF-induced corneal neovascularization. Structure activity studies suggest that thalidomide's anti-angiogenic activity is related to the open ring metabolites resulting from hydrolysis. Together these data support a correlation between thalidomide's antiangiogenic and teratogenic activities.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Teratogênicos
/
Talidomida
/
Neovascularização da Córnea
/
Córnea
Tipo de estudo:
Etiology_studies
/
Prognostic_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
1997
Tipo de documento:
Article