In:
Mediators of Inflammation, Hindawi Limited, Vol. 2015 ( 2015), p. 1-9
Abstract:
Allergic diseases, such as asthma and allergic rhinitis, are common. Therefore, the discovery of therapeutic drugs for these conditions is essential. Methyleugenol (ME) is a natural compound with antiallergic, antianaphylactic, antinociceptive, and anti-inflammatory effects. This study examined the antiallergic effect of ME on IgE-mediated inflammatory responses and its antiallergy mechanism in the mast cell line, RBL-2H3. We found that ME significantly inhibited the release of β -hexosaminidase, tumor necrosis factor- (TNF-) α , and interleukin- (IL-) 4, and was not cytotoxic at the tested concentrations (0–100 μ M). Additionally, ME markedly reduced the production of the proinflammatory lipid mediators prostaglandin E 2 (PGE 2 ), prostaglandin D 2 (PGD 2 ), leukotriene B 4 (LTB 4 ), and leukotriene C 4 (LTC 4 ). We further evaluated the effect of ME on the early stages of the Fc ε RI cascade. ME significantly inhibited Syk phosphorylation and expression but had no effect on Lyn. Furthermore, it suppressed ERK1/2, p38, and JNK phosphorylation, which is implicated in proinflammatory cytokine expression. ME also decreased cytosolic phospholipase A 2 (cPLA 2 ) and 5-lipoxygenase (5-LO) phosphorylation and cyclooxygenase-2 (COX-2) expression. These results suggest that ME inhibits allergic response by suppressing the activation of Syk, ERK1/2, p38, JNK, cPLA 2 , and 5-LO. Furthermore, the strong inhibition of COX-2 expression may also contribute to the antiallergic action of ME. Our study provides further information about the biological functions of ME.
Type of Medium:
Online Resource
ISSN:
0962-9351
,
1466-1861
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2015
detail.hit.zdb_id:
2008065-7
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