Objective:To evaluate the effect of standardized extract of Centella asiatica ECa 233 on inflammatory mediator production through cyclooxygenase-2(COX-2),extracellular signal-regulated kinase 1/2(ERK1/2)and nuclear fa...Objective:To evaluate the effect of standardized extract of Centella asiatica ECa 233 on inflammatory mediator production through cyclooxygenase-2(COX-2),extracellular signal-regulated kinase 1/2(ERK1/2)and nuclear factor-κB(NF-κB)pathway in keratinocyte Ha Ca T cells.Methods:Ha Ca T cells were treated with 0.1,1,10 and 100μg/m L ECa 233 in the presence of lipopolysaccharide(LPS).Proinflammatory cytokines and prostaglandin E2 were assessed with ELISA.Western blotting was used to determine the inhibition of COX-2,ERK1/2 and NF-κB protein expression.Results:ECa 233 suppressed LPS-induced release of interleukin-1β,tumor necrosis factor-α,and prostaglandin E2.ECa 233 also inhibited COX-2,phosphorylation of ERK1/2 and the activation of NF-κB.Moreover,the formation of reactive oxygen species(ROS)was decreased in response to LPS-inflamed keratinocytes.Conclusions:ECa 233 inhibits LPS-stimulated production of inflammatory mediators in keratinocytes via suppressing ERK1/2 and NF-κB pathways.The suppressive effect of ECa 233 may be related to an inhibition of ROS production.展开更多
基金supported by grant from the General Project and Invention of Prince of Songkla University(SCI600421S),Graduate School of Prince of Songkla University,Songkhla,Thailand.
文摘Objective:To evaluate the effect of standardized extract of Centella asiatica ECa 233 on inflammatory mediator production through cyclooxygenase-2(COX-2),extracellular signal-regulated kinase 1/2(ERK1/2)and nuclear factor-κB(NF-κB)pathway in keratinocyte Ha Ca T cells.Methods:Ha Ca T cells were treated with 0.1,1,10 and 100μg/m L ECa 233 in the presence of lipopolysaccharide(LPS).Proinflammatory cytokines and prostaglandin E2 were assessed with ELISA.Western blotting was used to determine the inhibition of COX-2,ERK1/2 and NF-κB protein expression.Results:ECa 233 suppressed LPS-induced release of interleukin-1β,tumor necrosis factor-α,and prostaglandin E2.ECa 233 also inhibited COX-2,phosphorylation of ERK1/2 and the activation of NF-κB.Moreover,the formation of reactive oxygen species(ROS)was decreased in response to LPS-inflamed keratinocytes.Conclusions:ECa 233 inhibits LPS-stimulated production of inflammatory mediators in keratinocytes via suppressing ERK1/2 and NF-κB pathways.The suppressive effect of ECa 233 may be related to an inhibition of ROS production.
