Division of Gastrointestinal Pathophysiology, Department of Bioscience, Institute of Natural Medicine, University of Toyama, Toyama 930-0194, Japan.
Biochem Biophys Res Commun. 2011 Dec 16;416(3-4):283-8. doi: 10.1016/j.bbrc.2011.11.014. Epub 2011 Nov 11.
Antigen-IgE-mediated mucosal mast-cell activation is critical in the development of food allergies. Cinnamaldehyde, a major constituent of Cinnamomi cortex, dose-dependently inhibited the antigen-IgE-induced degranulation of mucosal-type bone-marrow derived mast cells (mBMMCs) and RBL-2H3 cells. Cinnamaldehyde also suppressed the elevation of the intracellular Ca(2+) level that is induced by the extracellular Ca(2+) influx in antigen-IgE-stimulated mBMMCs. Furthermore, tyrosine phosphorylation of phospholipase C (PLC) γ1, which is a crucial activation switch for the intracellular Ca(2+) mobilization in mast cells, was attenuated by cinnamaldehyde. Together, our results demonstrated that cinnamaldehyde suppressed the intracellular Ca(2+) mobilization and the degranulation of mucosal mast cells by inhibiting the activity of the IgE receptor-PLCγ-Ca(2+) influx pathway. These findings suggest that cinnamaldehyde may have therapeutic potential in mucosal mast cell-related allergic diseases, such as food allergies.
抗原-IgE 介导体粘膜肥大细胞活化是食物过敏发展的关键。肉桂醛是肉桂皮的主要成分，它呈剂量依赖性地抑制了抗原-IgE 诱导的粘膜型骨髓来源的肥大细胞（mBMMC）和 RBL-2H3 细胞脱颗粒。肉桂醛还抑制了抗原-IgE 刺激的 mBMMC 中由细胞外 Ca2+内流引起的细胞内 Ca2+水平的升高。此外，PLCγ1 的酪氨酸磷酸化，这是肥大细胞中细胞内 Ca2+动员的关键激活开关，被肉桂醛减弱。总之，我们的研究结果表明，肉桂醛通过抑制 IgE 受体-PLCγ-Ca2+内流途径的活性，抑制了细胞内 Ca2+动员和粘膜肥大细胞的脱颗粒。这些发现表明，肉桂醛可能具有治疗与粘膜肥大细胞相关的过敏疾病（如食物过敏）的潜力。
