Spirulina maxima peptides suppress mast cell degranulation via inactivating Akt and MAPKs phosphorylation in RBL-2H3 cells

Vo, Thanh Sang; Kim, Young-Sang; Ngo, Dai Hung; Le, Phuong Uyen; Kim, Soyeon; Kim, Se‐Kwon

doi:10.1016/j.ijbiomac.2018.07.096

Cited by 19 publications

(12 citation statements)

References 19 publications

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“…Previous studies demonstrated that the formation of ROS and NLRP3 activation have been involved in mast cell degranulation. − Degranulation is the process of releasing mediators (histamine and β-Hexosaminidase) from the secretory granules within mast cells . Histamine and β-Hexosaminidase are presynthesized within mast cells and are degranulated by mast cells to release extracellular and other mediators involved in allergic reactions .…”

Section: Discussionmentioning

confidence: 99%

Sodium Sulfite-Induced Mast Cell Pyroptosis and Degranulation

Liu

Lü

Chen

et al. 2021

J. Agric. Food Chem.

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Sodium sulfite, a common food additive, has been proved to cause allergic reaction. Pyroptosis is an inflammatory form of programmed cell death with plasma membrane lysis. In this study, we found that sodium sulfite triggered pyroptosis, which depended on reactive oxygen species (ROS)/NOD-like receptor protein 3 (NLRP3) in RBL-2H3 mast cells. Sodium sulfite increased the generation of ROS and the expression of NLRP3, caspase-1, gasdermin D N-terminal (GSDMD-N), interleukin-1β (IL-1β), and interleukin-18 (IL-18). The ROS scavenger N-acetyl-L-carnosine (NAC) and the NLRP3 inhibitor MCC950 reversed these effects. Furthermore, using a lactate dehydrogenase kit, propidium iodide staining, scanning electron microscopy, colocalization of GSDMD-N with histamine, and neutral red staining, we found that sodium sulfite notably induced cell membrane rupture. Because β-Hexosaminidase and histamine play a key role in allergic reactions, we detected the release of β-Hexosaminidase and histamine. The data showed that the release of β-Hexosaminidase and histamine induced by sodium sulfite was increased with dose independence, which were inhibited after treatment with NAC or MCC950. Overall, evidence suggested that pyroptosis induced by sodium sulfite may rupture the cell membrane and result in degranulation of mast cells. Our study may provide new insights for the mechanism by which sodium sulfite induces mast cell death and sensitization.

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Section: Discussionmentioning

confidence: 99%

Sodium Sulfite-Induced Mast Cell Pyroptosis and Degranulation

Liu

Lü

Chen

et al. 2021

J. Agric. Food Chem.

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“…Activation of protein tyrosine kinases is the earliest detectable signaling response to FcεRI cross-linking on mast cells [26]. Upon tyrosine kinase activation, molecular mechanisms involving the Src family kinase Lyn [30] and/or intracellular signaling via MAPKs [26, 31] promotes mast cell degranulation. Mast cell activation inhibitors, including the corticosteroid dexamethasone [21], have been shown to suppress mast cell activation by down-regulating signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

“…Previous demonstrations showing that palbociclib can inhibit neoplastic mast cell proliferation [49] did not indicate whether palbociclib also inhibits mast cell activation, and specifically cell degradation, a key allergic disease treatment target. Hence, given palbociclib’s CDK inhibitory actions and its ability to suppress signaling molecule expression and/or activation, we hypothesize that palbociclib administered at a low-cytotoxicity dose may exert anti-IgE-mediated allergy effects by down-regulating of MAPK and/or NF-κB signaling downstream of CDK6 inhibition via FcεRI, whose activation may be modulated by the Src family kinase Lyn [30]. Lyn, interacting with FcεRIβ, is indispensable for FcεRI-mediated human mast cell activation, and specific inhibition of Lyn signaling may represent a new therapeutic strategy for the treatment of human allergic diseases [50].…”

Section: Discussionmentioning

confidence: 99%

CDK4/6 inhibitor palbociclib suppresses IgE-mediated mast cell activation

Hou

Sun

et al. 2019

J Transl Med

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Background Mast cell activation causes degranulation and release of cytokines, thereby promoting inflammation. The aim of this study was to investigate the inhibitory effect of CDK4/6 inhibition on mast cell activation in vitro and in vivo. Methods RBL-2H3 rat basophilic leukemia cells (BLCs) and mouse bone marrow-derived mast cells (BMMCs) were sensitized with anti-dinitrophenol (DNP) immunoglobulin (Ig)E antibodies, stimulated with DNP-human serum albumin (HSA) antigens, and treated with the CDK4/6 inhibitor palbociclib. Histological stains were applied to reveal cytomorphological changes. Murine IgE-mediated passive cutaneous anaphylaxis (PCA) and ovalbumin (OVA)-induced active systemic anaphylaxis (ASA) models were used to examine palbociclib effects on allergic reactions in vivo. Western blots were performed to detect the expression of cell signaling molecules associated with mast cell activation. Results Activated BLCs and BMMCs released copious granule-related mediators (histamine and β-hexosaminidase), which was reduced by palbociclib in a concentration-dependent manner. Palbociclib inhibited expression of the mast cell activation marker CD63 in activated BLCs and inhibited granule release (visualized with toluidine blue staining) while preventing morphological changes, (elongated shape maintained) and filamentous actin (F-actin) reorganization. Palbociclib suppressed molecular Lyn and/or mitogen-activated protein kinase (MAPK) signaling associated with mast cell activation in stimulated BLCs and attenuated allergic reactions in PCA mice dose dependently. Palbociclib attenuated body temperature reduction and diminished serum histamine levels in ovalbumin OVA-challenged ASA mice. Conclusion Palbociclib suppresses IgE-mediated mast cell activation in vitro and in vivo, suggesting that it may be developed into a therapy for mast cell-mediated allergic diseases via inhibition of mast cell degranulation.

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“…To further verify the relationship between Pts and LKB1/AMPK and FcεRI signaling, we used siRNA to knockdown LKB1. Akt is observed to be activated in response to IgE in mast cells . It has been reported that Pts reduces acetaminophen-induced liver injury by activating the AMPK/Akt pathway .…”

Section: Discussionmentioning

confidence: 99%

Pterostilbene Inhibits FcεRI Signaling through Activation of the LKB1/AMPK Pathway in Allergic Response

Wang

Jiang

et al. 2020

J. Agric. Food Chem.

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In this study, the role and mechanism of pterostilbene (Pts) in mast cell degranulation in vitro and in vivo were investigated. The results showed that Pts inhibited mast cell-mediated local passive allergic reactions in mice. In addition, treatment with Pts reduced both histamine release and calcium influx in rat peritoneal mast cells and RBL-2H3 cells and reduced IgE-mediated mast cell activation. Furthermore, the mechanism underlying Pts inhibition of mast cell signaling was probed via studying the effects of Pts on liver kinase B1 (LKB1), including the use of the LKB1 activator metformin and siRNA knockdown of LKB1. The data showed that Pts reduced the release of inflammatory mediators such as tumor necrosis factor-α, interleukin-6, leukotriene C4, and prostaglandin D2 in mast cells by activating the LKB1/adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway. Furthermore, Pts inhibited phosphorylation of FcεRI and FcεRI-mediated degranulation in RBL-2H3 cells. These effects were attenuated after LKB1 knockdown. Taken together, Pts could inhibit FcεRI signaling through activation of the LKB1/ AMPK signaling pathway in IgE-mediated mast cell activation. Thus, Pts might be an effective therapeutic agent for mast cellmediated allergic diseases.

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Spirulina maxima peptides suppress mast cell degranulation via inactivating Akt and MAPKs phosphorylation in RBL-2H3 cells

Cited by 19 publications

References 19 publications

Sodium Sulfite-Induced Mast Cell Pyroptosis and Degranulation

Sodium Sulfite-Induced Mast Cell Pyroptosis and Degranulation

CDK4/6 inhibitor palbociclib suppresses IgE-mediated mast cell activation

Pterostilbene Inhibits FcεRI Signaling through Activation of the LKB1/AMPK Pathway in Allergic Response

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