Abstract:
The target for the anti-inflammatory natural products like amentoflavone (2), which act by interfering with the proinflammatory cytokine pathway (e.g., TNF-α, IL-1β, 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.