Abstract
Aralia cordata is known in traditional Korean medicine as a remedy for arthritis. As a part of our program to screen medicinal plants for potential anti-inflammatory compounds, oleanoic acid 28-O-β-D-glycopyranosyl ester (OA) was isolated from the roots of Aralia cordata. So, the immune modulation molecular mechanism of OA isolated from A. cordata was studied.One of the possible mechanisms for its protective activities is by down regulation of the inflammatory responses. Therefore, cells from the human mast cell line (HMC-1) were used to investigate this effect. OA significantly inhibits the way in which phorbol 12-myristate 13-acetate (PMA) plus A23187 induces the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-8 and intracellular Ca2+ levels. In activated HMC-1 cells, phosphorylation of extra-signal response kinase (ERK) 1/2, degradation of IκB, and activation of NF-κB decreased after treatment with OA. OA suppressed the expression of TNF-α, IL-6 and IL-8 through a decrease in the intracellular levels of Ca2+ and ERK 1/2, as well as activation of NF-κB. These results indicated that OA exerted a regulatory effect on inflammatory reactions mediated by mast cells. Key words: Oleanoic acid 28-O-β-D-glycopyranosyl
Highlights
Mast cells are important effecter cells in the pathogenesis of allergic reactions and immune response system
The enhanced tumor necrosis factor (TNF)-α, IL-6, and IL-8 mRNA expression induced by phorbol 12-myristate 13-acetate (PMA) plus A23187 was inhibited by pretreatment of O-β-Dglycopyranosyl ester (OA) (Figure 3B)
In order to elucidate the mechanisms underlying the effects of OA, we examined the possible effects of OA on activation of MAP Kinases (MAPKs)
Summary
Mast cells are important effecter cells in the pathogenesis of allergic reactions and immune response system. Activated mast cells release pro-inflammatory cytokines and inflammatory mediators such as histamine, leukotrienes, serotonin, prostaglandin (PG)E2, and prostaglandin (PG)D2 (Zhu et al, 1999; Royer et al, 2001; Stassen et al, 2001) Cytokines such as interleukin (IL), tumor necrosis factor (TNF)-α, and IL-8 are released in a coordinate network and play an important role in chronic inflammation. TNF-α is an autocrine stimulator as well as a potent inducer of other inflammatory cytokines, including IL-1β, IL-6, IL-8, and granulocyte macrophage-colony stimulating factor (GM-CSF) (Arend and Dayer, 1995; Butler et al, 1995). Cytokines produce their cellular effects by activation of various transcription factors such as AP-1 and NF-κB. The inhibition of NF-κB can reduce the expression of inflammatory genes, and this is one of the mechanisms by which anti-inflammatory agents exert their anti-inflammatory effects (Newton et al, 1997)
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