Department of Herbal Pharmacology, College of Oriental Medicine, Kyung Hee University, Seoul, Republic of Korea.
Immunopharmacol Immunotoxicol. 2012 Aug;34(4):571-7. doi: 10.3109/08923973.2011.636048. Epub 2011 Dec 1.
The root of Angelica acutiloba is a widely used herbal medicine which has been used as a typical therapeutic for allergic diseases in traditional medicine. This study was aimed to investigate the effects of A. acutiloba on allergic reactions in in vitro and in vivo models and its mechanism of action. A. acutiloba was extracted by maceration with 80% ethanol (AAE) and standardized by high-performance liquid chromatography. We investigated the effect of AAE on phorbol-12-myristate-13-acetate plus calcium ionophore A23187 (PMACI)-induced cytokine release; phosphorylation of JNK, ERK, and p38 in human mast cell-1 (HMC-1); and compound 48/80-induced release of histamine in rat peritoneal mast cells (RPMCs). We also investigated the effects on Evans blue (EB) extravasation induced by anti-DNP IgE in rats. Treatment with 1, 10 and 100 μg/ml AAE concentration-dependently inhibited the release of cytokines (tumor necrosis factor-α, interleukin (IL) -6, and IL-8) and phosphorylation of ERK and JNK induced by PMACI in HMC-1 cells, but it did not inhibit the phosphorylation of p38. It also inhibited compound 48/80-induced histamine release in RPMCs. Oral administration of 271 mg/kg AAE inhibited EB extravasation in a passive cutaneous anaphylaxis rat model. In conclusion, AAE inhibited mast cell-derived allergic reactions by inhibiting the release of histamine, the production of pro-inflammatory cytokines, and the phosphorylation of ERK and JNK.
当归根是一种广泛使用的草药,在传统医学中被用作治疗过敏疾病的典型药物。本研究旨在探讨当归提取物(AAE)对体外和体内过敏反应模型的作用及其作用机制。AAE 用 80%乙醇(AAE)浸提,用高效液相色谱法进行标准化。我们研究了 AAE 对佛波醇-12-肉豆蔻酸-13-醋酸盐加钙离子载体 A23187(PMACI)诱导的细胞因子释放、人肥大细胞-1(HMC-1)中 JNK、ERK 和 p38 的磷酸化以及化合物 48/80 诱导的大鼠腹腔肥大细胞(RPMCs)中组胺释放的影响。我们还研究了 AAE 对大鼠抗-DNP IgE 诱导的 Evans 蓝(EB)渗出的影响。用 1、10 和 100μg/ml AAE 浓度依赖性抑制 PMACI 诱导的 HMC-1 细胞中细胞因子(肿瘤坏死因子-α、白细胞介素-6 和白细胞介素-8)释放和 ERK 和 JNK 的磷酸化,但不抑制 p38 的磷酸化。它还抑制化合物 48/80 诱导的 RPMCs 中组胺的释放。271mg/kg AAE 口服给药抑制被动皮肤过敏反应大鼠模型中的 EB 渗出。总之,AAE 通过抑制组胺释放、促炎细胞因子的产生以及 ERK 和 JNK 的磷酸化抑制肥大细胞来源的过敏反应。