Abstract
The target for the anti-inflammatory natural products like amentoflavone ( 2), which act by interfering with the proinflammatory cytokine pathway (e.g., TNF-alpha, IL-1beta, and NO synthase), is not yet well-defined. Data obtained from docking, electronic, and surface analyses shed some light on steric and electronic complementarity of these molecules to p38 MAPK, thereby suggesting a possible mechanism by which they might reduce the production of proinflammatory cytokines.
MeSH terms
-
Anti-Inflammatory Agents / chemistry*
-
Biflavonoids / chemistry
-
Cytokines / antagonists & inhibitors*
-
Flavanones / chemistry
-
Flavones / chemistry*
-
Flavonoids / chemistry
-
Glucosides / chemistry
-
Hydrogen Bonding
-
Imidazoles / chemistry*
-
Luteolin / chemistry
-
Models, Molecular*
-
Pyridines / chemistry*
-
Structure-Activity Relationship
-
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors*
-
p38 Mitogen-Activated Protein Kinases / chemistry
Substances
-
Anti-Inflammatory Agents
-
Biflavonoids
-
Cytokines
-
Flavanones
-
Flavones
-
Flavonoids
-
Glucosides
-
Imidazoles
-
Pyridines
-
isoginkgetin
-
luteolin-7-glucoside
-
p38 Mitogen-Activated Protein Kinases
-
naringenin
-
Luteolin
-
SB 203580
-
eriodictyol