SG-HQ2 inhibits mast cell-mediated allergic inflammation through suppression of histamine release and pro-inflammatory cytokines

Title
SG-HQ2 inhibits mast cell-mediated allergic inflammation through suppression of histamine release and pro-inflammatory cytokines
Author(s)
박필훈김상현[김상현]제인규[제인규]김희훈[김희훈]권택규[권택규]서승용[서승용]신태용[신태용]
Keywords
PASSIVE CUTANEOUS ANAPHYLAXIS; FACTOR-KAPPA-B; GALLIC ACID; CALCIUM; IL-6; IGE; EPIGALLOCATECHIN-3-GALLATE; RESPONSES; INNATE; MODEL
Issue Date
201505
Publisher
SAGE PUBLICATIONS LTD
Citation
EXPERIMENTAL BIOLOGY AND MEDICINE, v.240, no.5, pp.631 - 638
Abstract
In this study, we investigated the effect of 3,4,5-trihydroxy-N-(8-hydroxyquinolin-2-yl)benzamide) (SG-HQ2), a synthetic analogue of gallic acid (3,4,5-trihydroxybenzoic acid), on the mast cell-mediated allergic inflammation and the possible mechanism of action. Mast cells play major roles in immunoglobulin E-mediated allergic responses by the release of histamine, lipid-derived mediators, and pro-inflammatory cytokines. We previously reported the potential effects of gallic acid using allergic inflammation models. For incremental research, we synthesized the SG-HQ2 by the modification of functional groups from gallic acid. SG-HQ2 attenuated histamine release by the reduction of intracellular calcium in human mast cells and primary peritoneal mast cells. The inhibitory efficacy of SG-HQ2 was similar with gallic acid. Enhanced expression of pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1 beta, interleukin-4, and interleukin-6 in activated mast cells was significantly diminished by SG-HQ2 100 times lower concentration of gallic acid. This inhibitory effect was mediated by the reduction of nuclear factor-kappa B. In animal models, SG-HQ2 inhibited compound 48/80-induced serum histamine release and immunoglobulin E-mediated local allergic reaction, passive cutaneous anaphylaxis. Our results indicate that SG-HQ2, an analogue of gallic acid, might be a possible therapeutic candidate for mast cell-mediated allergic inflammatory diseases through suppression of histamine release and pro-inflammatory cytokines.
URI
http://hdl.handle.net/YU.REPOSITORY/32525http://dx.doi.org/10.1177/1535370214555663
ISSN
1535-3702
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약학대학 > 약학부 > Articles
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