Galangin attenuates mast cell-mediated allergic inflammation

Kim, Hui-Hun; Bae, Yunju; Kim, Sang-Hyun

doi:10.1016/j.fct.2013.03.015

Cited by 86 publications

(54 citation statements)

References 47 publications

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“…12 The blood from the mice was centrifuged at 400 g for 15 min at 4 C, and the serum was withdrawn to measure histamine content. HMC-1 cells (1 lmol/L) or compound 48/80 (5 lg/mL).…”

Section: Histamine Assaymentioning

confidence: 99%

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

Kim

Park

et al. 2014

Exp Biol Med (Maywood)

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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-a, interleukin-1b, 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-kB. 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 proinflammatory cytokines.

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“…12 The blood from the mice was centrifuged at 400 g for 15 min at 4 C, and the serum was withdrawn to measure histamine content. HMC-1 cells (1 lmol/L) or compound 48/80 (5 lg/mL).…”

Section: Histamine Assaymentioning

confidence: 99%

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

Kim

Park

et al. 2014

Exp Biol Med (Maywood)

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“…Subsequently, histamine is released and cytokines, chemokines, proteases and eicosanoids are secreted following the degranulation of mast cells (2). Histamine released from degranulated mast cells immediately initiates hypersensitivity and vasodilation and increases the permeability of vessels that have been exposed to external allergens (3). Pro-inflammatory cytokines secreted in mast cells, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 mediate the chronic inflammatory response (4).…”

Section: Introductionmentioning

confidence: 99%

“…RBL-2H3 cells (1x10 6 /well) were sensitized with anti-DNP IgE (10 µg/ml) and incubated overnight. Following pretreatment with or without formononetin (0.1, 1 and 10 µM) for 30 min according to previous studies (3,6), DNP-HSA (500 ng/ml) was added to the cells and they were incubated at 37˚C for 2 h. The cells were separated from the media by centrifugation at 400 x g for 5 min at 4˚C. The fluorescence intensity was determined using a fluorescence plate reader and the excitation and emission wavelengths were set at 360 and 440 nm, respectively.…”

Section: Introductionmentioning

confidence: 99%

Formononetin ameliorates mast cell‑mediated allergic inflammation via inhibition of histamine release and production of pro‑inflammatory cytokines

2017

Exp Ther Med

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Abstract. Various allergic diseases cause allergic inflammation, which is mediated by mast cells. The current study investigated the anti-allergic inflammatory effects of formononetin and its mechanism of action in vitro using mast cells. Levels of histamine and pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6, were measured to assess the effects of formononetin on allergic inflammation. The activation of intracellular calcium and nuclear factor (NF)-κB, as well as the activity of caspase-1, were assessed to determine the mechanism of action. It was determined that difference concentrations of formononetin (0.1, 1 and 10 µM) suppressed histamine release and secretion of TNF-α, IL-1β and IL-6. Further investigations indicated that the effects of formononetin were associated with a reduction of intracellular calcium, suppression of NF-κB activation and upstream IκKα phosphorylation and inhibition of caspase-1 activity. Therefore, the results of the current study demonstrated that formononetin ameliorated mast cell-mediated allergic inflammation.

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“…Previous studies have demonstrated that the flavonoid compounds used in the present study also have immunomodulatory, anti-inflammatory, and anti-proliferation properties that may be additional beneficial effects in allergic lung diseases (9,20,25). Evaluating these compounds for their chronic anti-inflammatory and antiproliferation properties in the airways would be an important complement to the present study.…”

Section: Discussionmentioning

confidence: 84%

Attenuation of airway smooth muscle contractility via flavonol-mediated inhibition of phospholipase-Cβ

Brown

Danielsson

Townsend

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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hanced contractility of airway smooth muscle (ASM) is a major pathophysiological characteristic of asthma. Expanding the therapeutic armamentarium beyond ␤-agonists that target ASM hypercontractility would substantially improve treatment options. Recent studies have identified naturally occurring phytochemicals as candidates for acute ASM relaxation. Several flavonoids were evaluated for their ability to acutely relax human and murine ASM ex vivo and murine airways in vivo and were evaluated for their ability to inhibit procontractile signaling pathways in human ASM (hASM) cells. Two members of the flavonol subfamily, galangin and fisetin, significantly relaxed acetylcholine-precontracted murine tracheal rings ex vivo (n ϭ 4 and n ϭ 5, respectively, P Ͻ 0.001). Galangin and fisetin also relaxed acetylcholine-precontracted hASM strips ex vivo (n ϭ 6 -8, P Ͻ 0.001). Functional respiratory in vivo murine studies demonstrated that inhaled galangin attenuated the increase in lung resistance induced by inhaled methacholine (n ϭ 6, P Ͻ 0.01). Both flavonols, galangin and fisetin, significantly inhibited purified phosphodiesterase-4 (PDE4) (n ϭ 7, P Ͻ 0.05; n ϭ 7, P Ͻ 0.05, respectively), and PLC␤ enzymes (n ϭ 6, P Ͻ 0.001 and n ϭ 6, P Ͻ 0.001, respectively) attenuated procontractile Gq agonists' increase in intracellular calcium (n ϭ 11, P Ͻ 0.001), acetylcholine-induced increases in inositol phosphates, and CPI-17 phosphorylation (n ϭ 9, P Ͻ 0.01) in hASM cells. The prorelaxant effect retained in these structurally similar flavonols provides a novel pharmacological method for dual inhibition of PLC␤ and PDE4 and therefore may serve as a potential treatment option for acute ASM constriction. bronchodilation; flexiVent; myograph; phosphodiesterase; phytochemical THERE ARE LIMITED PHARMACOLOGICAL options available to asthmatic patients that provide acute relaxation of airway smooth muscle (ASM). ␤-Agonists or anticholinergic medications remain the primary therapeutic classes of medications available for acute bronchodilation; however, in a growing number of patients frequent exacerbations remain a challenge. More recent formulations have combined long-acting ␤-agonists with inhaled steroids in an attempt to improve asthma symptomology. For example, in poorly controlled persistent asthmatic patients, the current recommendation is the addition of longacting ␤-agonist (LABA) to be used in combination with an inhaled corticosteroid. Somewhat paradoxically, when asthma exacerbations occur in patients treated with LABAs, they are often also administered a shorter acting member of the same drug class (i.e., short-acting ␤-adrenoceptor agonists). Thus clinicians heavily rely on ␤-agonists (both short and longacting), in both acute and chronic settings. This reliance has led to several concerns including the pathophysiological consequences of tolerance and airway hyperresponsiveness as well as a growing controversy regarding an association with negative clinical outcomes such as increased exacerbations and an increased risk of de...

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Galangin attenuates mast cell-mediated allergic inflammation

Cited by 86 publications

References 47 publications

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

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

Formononetin ameliorates mast cell‑mediated allergic inflammation via inhibition of histamine release and production of pro‑inflammatory cytokines

Attenuation of airway smooth muscle contractility via flavonol-mediated inhibition of phospholipase-Cβ

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