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Imidacloprid inhibits IgE-mediated RBL-2H3 cell degranulation and passive cutaneous anaphylaxis
被引:9
|作者:
Shi, Linbo
[1
]
Zou, Li
[1
,2
]
Gao, Jinyan
Xu, Huaing
[3
]
Shi, Xiaoyun
[4
]
Chen, Hongbing
[1
]
机构:
[1] Nanchang Univ, State Key Lab Food Sci & Technol, Nanchang 330047, Jiangxi, Peoples R China
[2] Nanchang Univ, Sch Food Sci, Nanchang 330047, Jiangxi, Peoples R China
[3] Nanchang Univ, Dept Rehabil, Affiliated Hosp 1, Nanchang 330006, Jiangxi, Peoples R China
[4] Nanchang Univ, Dept Anesthesiol, Affiliated Hosp 1, Nanchang 330006, Jiangxi, Peoples R China
基金:
国家高技术研究发展计划(863计划);
关键词:
Imidacloprid;
Mast cells;
Ca2+ influx;
D O I:
10.5415/apallergy.2016.6.4.236
中图分类号:
R392 [医学免疫学];
学科分类号:
100102 ;
摘要:
Background: Imidacloprid has been commonly used as a pesticide for crop protection and acts as nicotinic acetylcholine receptor agonists. Little information about the relationship between imidacloprid and allergy is available. Objective: This study aims to examine the effects of imidacoprid on IgE-mediated mast cell activation. Methods: The rat basophilic leukemia cell line RBL-2H3 (RBL-2H3 cells) were treated with 10(-3)-10(-12) mol/L imidacloprid, followed by measuring the mediator production, influx of Ca2+ in IgE-activated RBL-2H3 cells, and the possible effects of imidacoprid on antidinitrophenyl IgE-induced passive cutaneous anaphylaxis (PCA). Results: It was shown that imidacoprid suppressed the production of histamine, beta-hexosaminidase, leukotriene C4, interleukin-6, tumor necrosis factor-alpha, and Ca2+ mobilization in IgE-activated RBL-2H3 cells and decreased vascular extravasation in IgE-induced PCA. Conclusion: It is the first time to show that imidacloprid suppressed the activation of RBL-2H3 cells.
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页码:236 / 244
页数:9
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