Wang Hui-Na, Xiang Qiu-An, Lin Hao-Hui, Chen Jie-Ning, Guo Wen-Jie, Guo Wan-Meng, Yue Xiang-Ning, Zhao Zhen-Fu, Ji Kunmei, Chen Jia-Jie
Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Health Science Center, Shenzhen University, Shenzhen 518060, China.
Molecules. 2022 Feb 27;27(5):1577. doi: 10.3390/molecules27051577.
Mast cells (MCs) are an important treatment target for high-affinity IgE Fc receptor (FcεRI)-mediated allergic diseases. The plant-derived molecule 4-methylumbelliferone (4-MU) has beneficial effects in animal models of inflammation and autoimmunity diseases. The aim of this study was to examine 4-MU effects on MC activation and probe the underlying molecular mechanism(s). We sensitized rat basophilic leukemia cells (RBLs) and mouse bone marrow-derived mast cells (BMMCs) with anti-dinitrophenol (DNP) immunoglobulin (Ig)E antibodies, stimulated them with exposure to DNP-human serum albumin (HSA), and then treated stimulated cells with 4-MU. Signaling-protein expression was determined by immunoblotting. In vivo allergic responses were examined in IgE-mediated passive cutaneous anaphylaxis (PCA) and ovalbumin (OVA)-induced active systemic anaphylaxis (ASA) mouse models. 4-MU inhibited β-hexosaminidase activity and histamine release dose-dependently in FcεRI-activated RBLs and BMMCs. Additionally, 4-MU reduced cytomorphological elongation and F-actin reorganization while down-regulating IgE/Ag-induced phosphorylation of SYK, NF-κB p65, ERK1/2, p38, and JNK. Moreover, 4-MU attenuated the PCA allergic reaction (i.e., less ear thickening and dye extravasation). Similarly, we found that 4-MU decreased body temperature, serum histamine, and IL4 secretion in OVA-challenged ASA model mice. In conclusion, 4-MU had a suppressing effect on MC activation both in vitro and in vivo and thus may represent a new strategy for treating IgE-mediated allergic conditions.
肥大细胞(MCs)是高亲和力IgE Fc受体(FcεRI)介导的过敏性疾病的重要治疗靶点。植物衍生分子4-甲基伞形酮(4-MU)在炎症和自身免疫性疾病的动物模型中具有有益作用。本研究的目的是研究4-MU对MC激活的影响,并探究其潜在的分子机制。我们用抗二硝基苯酚(DNP)免疫球蛋白(Ig)E抗体使大鼠嗜碱性白血病细胞(RBLs)和小鼠骨髓来源的肥大细胞(BMMCs)致敏,用DNP-人血清白蛋白(HSA)刺激它们,然后用4-MU处理刺激后的细胞。通过免疫印迹法测定信号蛋白表达。在IgE介导的被动皮肤过敏反应(PCA)和卵清蛋白(OVA)诱导的主动全身过敏反应(ASA)小鼠模型中检测体内过敏反应。4-MU在FcεRI激活的RBLs和BMMCs中剂量依赖性地抑制β-己糖胺酶活性和组胺释放。此外,4-MU减少了细胞形态学伸长和F-肌动蛋白重组,同时下调了IgE/Ag诱导的SYK、NF-κB p65、ERK1/2、p38和JNK的磷酸化。此外,4-MU减轻了PCA过敏反应(即耳部增厚和染料外渗减少)。同样,我们发现4-MU降低了OVA激发的ASA模型小鼠的体温、血清组胺和IL4分泌。总之,4-MU在体外和体内对MC激活均有抑制作用,因此可能代表一种治疗IgE介导的过敏性疾病的新策略。