6533b7d0fe1ef96bd125af61

RESEARCH PRODUCT

Effect of triterpenoids on the inflammation induced by protein kinase C activators, neuronally acting irritants and other agents.

José-luis RíosAna-isabel HuguetRosa-maría GinerMaría Del Carmen RecioSalvador Máñez

subject

MezereinTime FactorsBryostatin 1ResiniferatoxinAnti-Inflammatory AgentsEnzyme ActivatorsPharmacologyBradykininchemistry.chemical_compoundGlucose OxidaseMiceAnimalsEdemaBryostatinRats WistarProtein kinase AProtein kinase CProtein Kinase CSkinPharmacologyNeurogenic inflammationArachidonic AcidMolecular StructureTerpenesBiological activityEarTriterpenesRatschemistryBiochemistryIrritantsDermatitis IrritantFemaleDiterpenesNeurogenic InflammationReactive Oxygen Species

description

In order to establish the mode of the anti-inflammatory activity of triterpenoids, 11 naturally occurring compounds were assayed on mouse ear oedema induced by the protein kinase C activators, mezerein, 12-O-tetradecanoylphorbol-13-acetate (TPA), two 12-deoxyphorbol-13-monoesters (13-tetradecanoate (DPT) and 13-phenylacetate (DPP)) and bryostatin 1, and by resiniferatoxin, xylene and arachidonic acid. The effects on bradykinin-induced paw oedema and on the rat skin inflammation caused by hydrogen peroxide were also examined. The oedema induced by mezerein and DPT was reduced to different extents by the triterpenoids administered epicutaneously (0.5 mg per ear). Against DPT-induced oedema, lupane and oleanane derivatives were the most effective compounds. Oleananes and lupanes possessing a carboxyl group were active against bryostatin 1-induced oedema. Most of the triterpenoids were ineffective against the neurogenic inflammation caused by resiniferatoxin and xylene. Many triterpenoids, especially oleanane and lupane alcoholic derivatives, were active against the plantar oedema induced by bradykinin and on the intradermal inflammation induced by hydrogen peroxide. In conclusion, the anti-inflammatory activity of triterpenoids may depend on inhibition of protein kinase C, without any involvement of neurogenic inflammatory mechanisms.

10.1016/s0014-2999(00)00860-8https://pubmed.ncbi.nlm.nih.gov/11134658