Isatins inhibit cyclooxygenase-2 and inducible nitric oxide synthase in a mouse macrophage cell line

Isatin is a versatile compound with a diversity of effects. We designed to investigate the inhibitory effect of isatin derivatives on lipopolysaccharide/interferon-γ-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins, production of prostaglandin E 2 (P...

Full description

Saved in:
Bibliographic Details
Published in:European journal of pharmacology 2007-02, Vol.556 (1), p.200-206
Main Authors: Matheus, Maria Eline, Violante, Flávio de Almeida, Garden, Simon John, Pinto, Angelo C., Fernandes, Patricia Dias
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cancer
Cell Line
Cell Survival - drug effects
Chemoprevention
Cyclooxygenase 2 - metabolism
Cyclooxygenase Inhibitors - pharmacology
Cyclooxygenase-2
Inducible nitric oxide synthase
Isatin
Isatin - pharmacology
Lipopolysaccharides - pharmacology
Macrophages - drug effects
Macrophages - enzymology
Medical sciences
Mice
Nitric Oxide - biosynthesis
Nitric Oxide Synthase Type II - antagonists & inhibitors
Nitric Oxide Synthase Type II - metabolism
Pharmacology. Drug treatments
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Isatin is a versatile compound with a diversity of effects. We designed to investigate the inhibitory effect of isatin derivatives on lipopolysaccharide/interferon-γ-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins, production of prostaglandin E 2 (PGE 2), nitric oxide (NO), tumor necrosis factor (TNF-α), and their capacity to scavenge NO. Isatins inhibit TNF-α production and iNOS and COX-2 protein expression resulting on reduced levels of NO and PGE 2. Our results indicate isatin and it derivatives as inhibitors of iNOS and COX-2 enzymes, which might be used as anti-inflammatory and antitumoral agents.
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2006.10.057