Effect of oxygen–glucose deprivation on degranulation and histamine release of mast cells

Shen, Yao; Fu, Qiang; Dai, Haibin; Tu, Hongming; Wei, Er-Qing; Luo, Jianhong; Chen, Zhong

doi:10.1007/s00441-005-0041-z

Cited by 15 publications

(13 citation statements)

References 26 publications

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“…In accordance with previous findings, the amplitude of MCs degranulation is dependent on the duration of anoxic insult (Hu et al, 2005). Degranulation was accompanied by significant leakage of LDH, indicating a cytotoxic effect induced by OGD.…”

Section: Discussionsupporting

confidence: 92%

“…Cultured MC/9 cells were exposed to 3, 6, 8, or 16 h of OGD, then harvested and processed. As pointed out by previous studies on primary rat MCs, OGD induced mastocytic activation (Hu et al, 2005). When stained with toluidine blue and observed by light microscopy, most MC/9 cells in the control group showed metachromatic granules and membrane integrity (Fig.…”

Section: Ogd Promotes Mc/9 Cells Activationsupporting

confidence: 63%

“…MC/9 cells were fixed with Immunofix (Bio-Optica, Milano, Italy) and stained with 0.005% toluidine blue pH 2.5 (Merck, Darmstadt, Germany). The number of degranulated MCs was counted under a light microscope, considering degranulated the cells showing lack of cellular periphery integrity, pale purple staining or extrusion of granules out of the cells (Hu et al, 2005). The numbers of degranulated and total MCs were assessed from three randomly selected areas counting a minimum of 300 cells/field.…”

Section: Preparation Of Mc/9-conditioned Medium (Cm)mentioning

confidence: 99%

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PEA and luteolin synergistically reduce mast cell-mediated toxicity and elicit neuroprotection in cell-based models of brain ischemia

et al. 2016

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a b s t r a c tThe combination of palmitoylethanolamide (PEA), an endogenous fatty acid amide belonging to the family of the N-acylethanolamines, and the flavonoid luteolin has been found to exert neuroprotective activities in a variety of mouse models of neurological disorders, including brain ischemia. Indirect findings suggest that the two molecules can reduce the activation of mastocytes in brain ischemia, thus modulating crucial cells that trigger the inflammatory cascade. Though, no evidence exists about a direct effect of PEA and luteolin on mast cells in experimental models of brain ischemia, either used separately or in combination. In order to fill this gap, we developed a novel cell-based model of severe brain ischemia consisting of primary mouse cortical neurons and cloned mast cells derived from mouse fetal liver (MC/9 cells) subjected to oxygen and glucose deprivation (OGD).OGD exposure promoted both mast cell degranulation and the release of lactate dehydrogenase (LDH) in a time-dependent fashion. MC/9 cells exacerbated neuronal damage in neuron-mast cells co-cultures exposed to OGD. Likewise, the conditioned medium derived from OGD-exposed MC/9 cells induced significant neurotoxicity in control primary neurons. PEA and luteolin pre-treatment synergistically prevented the OGD-induced degranulation of mast cells and reduced the neurotoxic potential of MC/9 cells conditioned medium. Finally, the association of the two drugs promoted a direct synergistic neuroprotection even in pure cortical neurons exposed to OGD.In summary, our results indicate that mast cells release neurotoxic factors upon OGD-induced activation. The association PEA-luteolin actively reduces mast cell-mediated neurotoxicity as well as pure neurons susceptibility to OGD.

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Section: Discussionsupporting

confidence: 92%

Section: Ogd Promotes Mc/9 Cells Activationsupporting

confidence: 63%

Section: Preparation Of Mc/9-conditioned Medium (Cm)mentioning

confidence: 99%

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PEA and luteolin synergistically reduce mast cell-mediated toxicity and elicit neuroprotection in cell-based models of brain ischemia

et al. 2016

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“…Cardiac MCs accumulated in massive numbers in the infarct region after acute myocardial infarction [Engels et al, 1995] and can rapidly degranulate, releasing histamine, tumor necrosis factor (TNF)-␣ and thromboxane B 2 shortly after myocardial ischemia [Frangogiannis et al, 1998]. Similarly, oxygen-glucose deprivation induces MCs to degranulate [Hu et al, 2005].…”

mentioning

confidence: 99%

Mast Cell Stabilization Limits Hypoxic-Ischemic Brain Damage in the Immature Rat

Jin¹,

Silverman²,

Vannucci

2007

Dev Neurosci

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Perinatal hypoxic-ischemic (HI) brain damage is a major cause of mortality and neurological morbidity in infants and children. Using an established model of unilateral hypoxia-ischemia in neonatal rats, the present study focused on mast cells (MCs), important regulators of inflammatory processes, as potential contributors to HI damage. MCs are present in the pia of the neonatal rat, entering the central nervous system (CNS) during cerebral development along penetrating blood vessels. Following hypoxia-ischemia, MC numbers increased dramatically in the ipsilateral (ischemic) hemisphere (p < 0.01). In animals exposed to hypoxia only, the numbers of MCs were elevated in both hemispheres to an extent equal to that observed in the contralateral hemisphere of HI animals (p < 0.05 vs. control). Within damaged areas (ipsilateral only), MCs were observed in regions of activated microglia and astroglia that characterize the ischemic hemisphere. Using a triple-label paradigm, MCs were observed along elongating blood vessels, some of which express the GLUT1 isoform of the glucose transporter protein, indicative of blood-brain barrier vessels. To determine whether MC activation has a role in HI brain damage, rat pups were treated with the MCs stabilizer, disodium cromoglycate (cromolyn),prior to and/or following hypoxia-ischemia. The cromolyn treatment inhibited MC migration into the CNS (p < 0.05) and limited brain damage more than 50% (p < 0.01) vs. saline controls. These data support the hypothesis that MCs are key contributors to the extent of brain damage due to hypoxia-ischemia in the immature animal.

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“…8 In ischemic experiments in vitro, mast cells degranulate and release histamine following oxygen-glucose deprivation (OGD). 9 Taken together, these studies suggest that mast cells and histamine from mast cells may play a crucial role in the pathological process of ischemia, and mast cell manipulation using therapeutic agents would be a logical step toward clinical management of ischemia.…”

Section: Introductionmentioning

confidence: 97%

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

Shen

Zhang

et al. 2007

Cell Biochemistry & Function

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Carnosine (beta-alanyl-histidine) is a naturally occurring dipeptide that has been characterized as a putative hydrophilic antioxidant. The protective function of carnosine has been demonstrated in neuronal cells under ischemic injury. The purpose of this study was to investigate the effects of carnosine on oxygen-glucose deprivation (OGD)-induced degranulation and histamine release from mast cells. Cultured mast cells were exposed to OGD for 4 h, and then the degranulation was observed immediately by microscopy. Histamine release was analyzed by high-performance liquid chromatography (HPLC). OGD caused degranulation of mast cells, and increased histamine and lactate dehydrogenase (LDH) release. Carnosine (at a concentration of 5 mM) alone did not produce any appreciable effect on degranulation, histamine, and LDH release from mast cells under normal condition, but significantly inhibited the degranulation, histamine, and LDH release of mast cells induced by OGD. These results indicate that carnosine can protect mast cells from degranulation and histamine release and it may be an endogenous mast cell stabilizer in the pathological processes induced by ischemia.

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Effect of oxygen–glucose deprivation on degranulation and histamine release of mast cells

Cited by 15 publications

References 26 publications

PEA and luteolin synergistically reduce mast cell-mediated toxicity and elicit neuroprotection in cell-based models of brain ischemia

PEA and luteolin synergistically reduce mast cell-mediated toxicity and elicit neuroprotection in cell-based models of brain ischemia

Mast Cell Stabilization Limits Hypoxic-Ischemic Brain Damage in the Immature Rat

Carnosine attenuates mast cell degranulation and histamine release induced by oxygen–glucose deprivation

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