Inhibitory Effect ofRubus Coreanuson Compound 48/80- or Anti-DNP IgE-Induced Mast Cell Activation

2004 ◽  
Vol 4 (2) ◽  
pp. 100
Author(s):  
Guang Zhao Li ◽  
Ok Hee Chai ◽  
Chang Ho Song
Molecules ◽  
2020 ◽  
Vol 25 (23) ◽  
pp. 5580
Author(s):  
Lorina I. Badger-Emeka ◽  
Promise Madu Emeka ◽  
Krishnaraj Thirugnanasambantham ◽  
Hairul Islam M. Ibrahim

Allergy is an immunological disorder that develops in response to exposure to an allergen, and histamines mediate these effects via histidine decarboxylase (HDC) activity at the intracellular level. In the present study, we developed a 3D model of Klebsiella pneumoniae histidine decarboxylase (HDC) and analyzed the HDC inhibitory potential of cinnamaldehyde (CA) and subsequent anti-allergic potential using a bacterial and mammalian mast cell model. A computational and in vitro study using K. pneumonia revealed that CA binds to HDC nearby the pyridoxal-5′-phosphate (PLP) binding site and inhibited histamine synthesis in a bacterial model. Further study using a mammalian mast cell model also showed that CA decreased the levels of histamine in the stimulated RBL-2H3 cell line and attenuated the release of β-hexoseaminidase and cell degranulation. In addition, CA treatment also significantly suppressed the levels of pro-inflammatory cytokines TNF-α and IL-6 and the nitric oxide (NO) level in the stimulated mast cells. A gene expression and Western blotting study revealed that CA significantly downregulated the expressions of MAPKp38/ERK and its downstream pro-allergic mediators that are involved in the signaling pathway in mast cell cytokine synthesis. This study further confirms that CA has the potential to attenuate mast cell activation by inhibiting HDC and modifying the process of allergic disorders.


2015 ◽  
Vol 406 (1-2) ◽  
pp. 263-271 ◽  
Author(s):  
Yue Lu ◽  
Shuangfan Cai ◽  
Hongsheng Tan ◽  
Wenwei Fu ◽  
Hong Zhang ◽  
...  

2011 ◽  
Vol 59 (10) ◽  
pp. 5595-5601 ◽  
Author(s):  
Tomoko Horiguchi ◽  
Nahoko Ishiguro ◽  
Kazuyasu Chihara ◽  
Kazuhiro Ogi ◽  
Kenji Nakashima ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Rafael Bonamichi-Santos ◽  
Marcelo Vivolo Aun ◽  
Jorge Kalil ◽  
Mariana Concepcion Castells ◽  
Pedro Giavina-Bianchi

Programmed cell death ligand 1(PDL-1) is known for its inhibitory effect on the cellular immune response. Even though it is expressed on the surface of mast cells, its role in allergic diseases is unknown. We analyzed the effects of PD-L1 blockade in a murine model of active cutaneous anaphylaxis (ACA). C57BL/6 mice were sensitized and challenged with ovalbumin (OVA). Blood samples were collected to measure specific immunoglobulins. The mice were divided into six groups that underwent the active cutaneous anaphylaxis procedure. Group 1 (negative control) received 50 μl of phosphate-buffered saline (PBS) subcutaneously, and the other five groups were sensitized with 50 μg of OVA subcutaneously. Group 2 was the positive control, and the others received the anti-PD-L1 antibody or its isotype during sensitization (groups 3 and 4) or during the challenge (groups 5 and 6). All animals that underwent ACA on the ears with OVA and PBS were sacrificed, and the reaction was evaluated by extravasation of Evans blue (measured by spectrophotometry) and histological analysis of the collected fragments. Anti-PD-L1 blockade during the sensitization phase led to a reduction in specific IgE and IgG1 levels, allergic reaction intensity at the ACA site, and mast cell degranulation in the tissue. There was no significant biological effect of anti-PD-L1 administration on the challenge phase. PD-L1 blockade during allergen sensitization inhibited the synthesis of specific IgE and IgG1 and decreased mast cell activation in this murine model of anaphylaxis.


2019 ◽  
Vol 71 ◽  
pp. 205-214 ◽  
Author(s):  
Shunli Pan ◽  
Xiaoxia Zhao ◽  
Ning Ji ◽  
Chen Shao ◽  
Bingjie Fu ◽  
...  

2016 ◽  
Vol 27 ◽  
pp. 631-644 ◽  
Author(s):  
Myungsuk Kim ◽  
Sun Young Kim ◽  
Ahmad Randy ◽  
Sue Ji Lim ◽  
Banzragch Dorjsembe ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Peeraphong Lertnimitphun ◽  
Wenhui Zhang ◽  
Wenwei Fu ◽  
Baican Yang ◽  
Changwu Zheng ◽  
...  

IntroductionAsthma is a chronic and recurring airway disease, which related to mast cell activation. Many compounds derived from Chinese herbal medicine has promising effects on stabilizing mast cells and decreasing inflammatory mediator production. Safranal, one of the active compounds from Crocus sativus, shows many anti-inflammatory properties. In this study, we evaluated the effect of safranal in ovalbumin (OVA)-induced asthma model. Furthermore, we investigate the effectiveness of safranal on stabilizing mast cell and inhibiting the production of inflammatory mediators in passive systemic anaphylaxis (PSA) model.MethodsOVA-induced asthma and PSA model were used to evaluate the effect of safranal in vivo. Lung tissues were collected for H&E, TB, IHC, and PAS staining. ELISA were used to determine level of IgE and chemokines (IL-4, IL-5, TNF-α, and IFN-γ). RNA sequencing was used to uncovers genes that safranal regulate. Bone marrow-derived mast cells (BMMCs) were used to investigate the inhibitory effect and mechanism of safranal. Cytokine production (IL-6, TNF-α, and LTC4) and NF-κB and MAPKs signaling pathway were assessed.ResultsSafranal reduced the level of serum IgE, the number of mast cells in lung tissue were decreased and Th1/Th2 cytokine levels were normalized in OVA-induced asthma model. Furthermore, safranal inhibited BMMCs degranulation and inhibited the production of LTC4, IL-6, and TNF-α. Safranal inhibits NF-κB and MAPKs pathway protein phosphorylation and decreases NF-κB p65, AP-1 nuclear translocation. In the PSA model, safranal reduced the levels of histamine and LTC4 in serum.ConclusionsSafranal alleviates OVA-induced asthma, inhibits mast cell activation and PSA reaction. The possible mechanism occurs through the inhibition of the MAPKs and NF-κB pathways.


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