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Objective:The anti-inflammatory effects of Ecklonia cava(EC)and its mechanism of action were examined in phorbol-12 myristate 13-acetate(30 nmol/L)and A23187(1μmol/L)(PMACI)stimulated human mast cell line-1 cells.Methods:Nitric oxide content,inducible nitric oxide synthase and cyclooxygenase-2 protein expression,pro-inflammatory cytokines including IL-1β,TNF-α,and IL-6 mRNA and protein expressions were determined.In addition,extracellular regulated protein kinases/mitogen-activated protein kinase(ERK/MAPK)activation was examined.Results:EC dose-dependently suppressed inducible nitric oxide synthase and cyclooxygenase-2 protein expression and subsequently it reduces nitric oxide content in PMACI stimulated human mast cell line-1 cells.EC dose-dependently inhibited the mRNA as well as protein expression of TNF-α,IL—1β,and TL-6 in the PMACI stimulated human mast cell line-1 cells without any cytotoxic effect.Furthermore,EC significantly inhibited PMACI induced phosphorylation of ERK1/2 in a dose-dependent manner without affecting the total protein levels.Conclusions:EC exert its anti-inflammatory actions via inhibition of ERK/MAPK signalling pathway,suggesting that EC is a potent and efficacious anti-inflammatory agent for mast cellmediated inflammatory diseases.
Objective: The anti-inflammatory effects of Ecklonia cava (EC) and its mechanism of action were examined in phorbol-12 myristate 13-acetate (30 nmol / L) and A23187 1 cells. Methods: Nitric oxide content, inducible nitric oxide synthase and cyclooxygenase-2 protein expression, pro-inflammatory cytokines including IL-1β, TNF-α, and IL-6 mRNA and protein expressions were determined. Results: EC dose-dependently suppressed inducible nitric oxide synthase and cyclooxygenase-2 protein expression and subsequently it reduces nitric oxide content in PMACI stimulated human mast cell line-1 cells .EC dose-dependently inhibited the mRNA as well as protein expression of TNF-α, IL-1β, and TL-6 in the PMACI stimulated human mast cell line-1 cells without any cytotoxic effect. Durthermore, EC significantly inhibited PMACI induced phosphorylation of ER Suggesting that EC is a potent and efficacious anti-inflammatory agent for mast cellmediated inflammatory diseases.