title: Inhibitory effect of methyleugenol on IgE-mediated allergic inflammation in RBL-2H3 cells.
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 μM). Additionally, ME markedly reduced the production of the proinflammatory lipid mediators prostaglandin E2 (PGE2), prostaglandin D2 (PGD2), leukotriene B4 (LTB4), and leukotriene C4 (LTC4). We further evaluated the effect of ME on the early stages of the FcεRI 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 A2 (cPLA2) 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, cPLA2, 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.
authors.affiliation: School of Traditional Chinese Medical Sciences, Southern Medical University, Guangzhou 510515, China ; Guangdong Province Key Laboratory of Chinese Medicine Pharmaceutics, Southern Medical University, Guangzhou 510515, China.
authors.forename: Feng
authors.identifier: 0000-0002-3091-7528
authors.initials: F
authors.lastname: Tang
authors.affiliation: School of Traditional Chinese Medical Sciences, Southern Medical University, Guangzhou 510515, China ; Guangdong Province Key Laboratory of Chinese Medicine Pharmaceutics, Southern Medical University, Guangzhou 510515, China.
authors.forename: Feilong
authors.identifier: 0000-0002-2605-4168
authors.initials: F
authors.lastname: Chen
authors.affiliation: School of Traditional Chinese Medical Sciences, Southern Medical University, Guangzhou 510515, China ; Guangdong Province Key Laboratory of Chinese Medicine Pharmaceutics, Southern Medical University, Guangzhou 510515, China.
authors.forename: Xiao
authors.identifier: 0000-0002-5630-8907
authors.initials: X
authors.lastname: Ling
authors.affiliation: School of Traditional Chinese Medical Sciences, Southern Medical University, Guangzhou 510515, China ; Guangdong Province Key Laboratory of Chinese Medicine Pharmaceutics, Southern Medical University, Guangzhou 510515, China.
authors.forename: Yao
authors.identifier: 0000-0002-1946-2059
authors.initials: Y
authors.lastname: Huang
authors.affiliation: School of Traditional Chinese Medical Sciences, Southern Medical University, Guangzhou 510515, China ; Guangdong Province Key Laboratory of Chinese Medicine Pharmaceutics, Southern Medical University, Guangzhou 510515, China.
authors.forename: Xiaomei
authors.identifier: 0000-0003-4719-9494
authors.initials: X
authors.lastname: Zheng
authors.affiliation: School of Traditional Chinese Medical Sciences, Southern Medical University, Guangzhou 510515, China ; Guangdong Province Key Laboratory of Chinese Medicine Pharmaceutics, Southern Medical University, Guangzhou 510515, China.
authors.forename: Qingfa
authors.identifier: 0000-0001-9965-1150
authors.initials: Q
authors.lastname: Tang
authors.affiliation: School of Traditional Chinese Medical Sciences, Southern Medical University, Guangzhou 510515, China ; Guangdong Province Key Laboratory of Chinese Medicine Pharmaceutics, Southern Medical University, Guangzhou 510515, China.
authors.forename: Xiaomei
authors.identifier: 0000-0002-5797-6763
authors.initials: X
authors.lastname: Tan
mesh_terms: D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism; D045744:Cell Line, Tumor; D019069:Cell Respiration; D015232:Dinoprostone / Q000378:metabolism; D005054:Eugenol / Q000031:analogs & derivatives* / Q000737:chemistry; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D006967:Hypersensitivity / Q000276:immunology*; D007124:Immunoenzyme Techniques; D007073:Immunoglobulin E / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D015847:Interleukin-4 / Q000378:metabolism; D007975:Leukotriene B4 / Q000378:metabolism; D017997:Leukotriene C4 / Q000378:metabolism; D008407:Mast Cells / Q000166:cytology; D009153:Mutagens; D015230:Prostaglandin D2 / Q000378:metabolism; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D001619:beta-N-Acetylhexosaminidases / Q000378:metabolism
chemical_list: D009153:Mutagens; D014409:Tumor Necrosis Factor-alpha; D007975:Leukotriene B4; D015847:Interleukin-4; D016718:Arachidonic Acid; C005223:methyleugenol; D017997:Leukotriene C4; D007073:Immunoglobulin E; D005054:Eugenol; D048049:Extracellular Signal-Regulated MAP Kinases; D001619:beta-N-Acetylhexosaminidases; D015232:Dinoprostone; D015230:Prostaglandin D2