|国家科技期刊平台
首页|期刊导航|中国免疫学杂志|苦精促进MrgprB2介导的鼠肥大细胞脱颗粒

苦精促进MrgprB2介导的鼠肥大细胞脱颗粒OA北大核心CSTPCD

Denatonium benzoate promotes MrgprB2-mediated rat mast cell degranulation

中文摘要英文摘要

目的:探讨微污染物苯甲地那铵(DB)对鼠Mas相关G蛋白偶联受体B2(MrgprB2)介导的肥大细胞(MCs)脱颗粒的影响,以较全面评估DB与以MCs脱颗粒为基础的过敏性疾病之间的关系.方法:建立MrgprB2介导的体外大鼠嗜碱性细胞白血病细胞株(RBL-2H3)活化模型,用不同剂量DB与RBL-2H3细胞共同孵育过夜,加入MrgprB2配体P物质(SP)按不同检测目的刺激RBL-2H3细胞不同时间后收集细胞或上清液,底物法检测MCs颗粒物质如β-氨基己糖苷酶(β-hex),ELISA检测白三烯C4(LTC4)、IL-6、TNF-α及细胞质磷脂酶A2(cPLA2)活性,荧光法检测MCs Ca2+内流与细胞MrgprB2受体表达的变化.结果:10 μmol/L、50 μmol/L、80 μmol/L、100 μmol/L DB能促进MrgprB2介导的RBL-2H3细胞活化时β-hex、LTC4释放,且这一过程伴有细胞内Ca2+内流的增加,且其效应呈一定的剂量依赖关系.此外,DB预处理对RBL-2H3内TNF-α和IL-6释放无影响,且不影响RBL-2H3上MrgprB2的表达增加.结论:DB促进MrgprB2介导的RBL-2H3细胞活化脱颗粒,其机制可能与通过促进MrgprB2中通路Ca2+信号活化有关.

Objective:To explore the potent effects of denatonium benzoate(DB)on Mas-related G protein-coupled receptor-B2(MrgprB2)-mediated rat mast cell degranulation.Methods:RBL-2H3 cells were treated with DB overnight,before challenged with MrgprB2 ligands substance P(SP).The release of β-hex from MrgprB2-activated RBL-2H3 was detected by substrate method.Detec-tion of LTC4,IL-6,TNF-α and cPLA2 activity were performed by ELISA.The Ca2+influx and the expression of RBL-2H3 MrgprB2 re-ceptors were measured by fluorescence assay.Results:The results showed 10 μmol/L,50 μmol/L,80 μmol/L,100 μmol/L DB treat-ments promoted β-hex and LTC4 releases from activated RBL-2H3,accompanied by increased Ca2+mobilization and cPLA2 activa-tion.DB treatments did not affect IL-6 and TNF-α LTC4 releases in MrgprB2-activated RBL-2H3,as well as the levels of MrgprB2 ex-pression in mast cells.Conclusion:Taken together,DB enhanced the MrgprB2-mediated RBL-2H3 degranulation in vitro,probably by up-regulating Ca2+mobilization in activated cells.

徐华平;石小云;邹节新;李欣;谢梦婷;肖诗宇;石林波

南昌大学第一附属医院,南昌 330006南昌大学医学部基础医学院,南昌 330046南昌大学食品学院,南昌 330006南昌大学医学部第一临床医学院,南昌 330006

基础医学

苯甲地那铵MrgprB2肥大细胞脱颗粒Ca2+活化

Denatonium benzoateMrgprB2Mast cell degranulationCa2+mobilization

《中国免疫学杂志》 2024 (010)

2037-2041 / 5

国家自然科学基金项目(21866020,32060306);江西省自然科学基金(20202BABL206108).

10.3969/j.issn.1000-484X.2024.10.003

评论