Kim Yeon-Yong, Je In-Gyu, Kim Min Jong, Kang Byeong-Cheol, Choi Young-Ae, Baek Moon-Chang, Lee Byungheon, Choi Jin Kyeong, Park Hae Ran, Shin Tae-Yong, Lee Soyoung, Yoon Seung-Bin, Lee Sang-Rae, Khang Dongwoo, Kim Sang-Hyun
CMRI, Department of Pharmacology, Daegu 700-422, Republic of Korea.
Department of Molecular Medicine, Daegu 700-422, Republic of Korea.
Acta Pharmacol Sin. 2017 Jan;38(1):90-99. doi: 10.1038/aps.2016.112. Epub 2016 Nov 28.
Mast cells are important effector cells in immunoglobulin (Ig) E-mediated allergic reactions such as asthma, atopic dermatitis and rhinitis. Vanillic acid, a natural product, has shown anti-oxidant and anti-inflammatory activities. In the present study, we investigated the anti-allergic inflammatory effects of ortho-vanillic acid (2-hydroxy-3-methoxybenzoic acid, o-VA) that was a derivative of vanillic acid isolated from Amomum xanthioides. In mouse anaphylaxis models, oral administration of o-VA (2, 10, 50 mg/kg) dose-dependently attenuated ovalbumin-induced active systemic anaphylaxis and IgE-mediated cutaneous allergic reactions such as hypothermia, histamine release, IgE production and vasodilation; administration of o-VA also suppressed the mast cell degranulator compound 48/80-induced anaphylaxis. In cultured mast cell line RBL-2H3 and isolated rat peritoneal mast cells in vitro, pretreatment with o-VA (1-100 μmol/L) dose-dependently inhibited DNP-HSA-induced degranulation of mast cells by decreasing the intracellular free calcium level, and suppressed the expression of pro-inflammatory cytokines TNF-α and IL-4. Pretreatment of RBL-2H3 cells with o-VA suppressed DNP-HSA-induced phosphorylation of Lyn, Syk, Akt, and the nuclear translocation of nuclear factor-κB. In conclusion, o-VA suppresses the mast cell-mediated allergic inflammatory response by blocking the signaling pathways downstream of high affinity IgE receptor (FcεRI) on the surface of mast cells.
肥大细胞是免疫球蛋白(Ig)E介导的过敏反应(如哮喘、特应性皮炎和鼻炎)中的重要效应细胞。香草酸是一种天然产物,已显示出抗氧化和抗炎活性。在本研究中,我们研究了从益智中分离得到的香草酸衍生物邻香草酸(2-羟基-3-甲氧基苯甲酸,o-VA)的抗过敏炎症作用。在小鼠过敏反应模型中,口服o-VA(2、10、50mg/kg)剂量依赖性地减轻卵清蛋白诱导的主动全身过敏反应以及IgE介导的皮肤过敏反应,如体温过低、组胺释放、IgE产生和血管舒张;给予o-VA还可抑制肥大细胞脱颗粒剂化合物48/80诱导的过敏反应。在体外培养的肥大细胞系RBL-2H3和分离的大鼠腹膜肥大细胞中,用o-VA(1-100μmol/L)预处理剂量依赖性地抑制DNP-HSA诱导的肥大细胞脱颗粒,通过降低细胞内游离钙水平,并抑制促炎细胞因子TNF-α和IL-4的表达。用o-VA预处理RBL-2H3细胞可抑制DNP-HSA诱导的Lyn、Syk、Akt磷酸化以及核因子κB的核转位。总之,o-VA通过阻断肥大细胞表面高亲和力IgE受体(FcεRI)下游的信号通路来抑制肥大细胞介导的过敏炎症反应。