Samultang has been believed for prevention and remedy various blood diseases such asmenstrual irregularity, anemia, and metrorrhagia. However, the mechanism that accounts foranti-inflammatory effects of the Samultang is still not fully understood. This study was designedto evaluate whether and how the Samultang could modulate the production of pro-inflammatorycytokines in phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187 treated-human mast cell line, HMC-1. Samultang inhibited the production of tumor necrosis factor(TNF)-α, interleukin (IL)-6, granulocyte macrophage colony stimulating factor (GM-CSF), andvascular endothelial growth factor (VEGF) in HMC-1. Maximal inhibition rate of TNF-α, IL-6, GM-CSF,and VEGF by 0.1 mg/ml Samultang was about 70.73 ± 3.0%, 51.49 ± 4.14%, 54.03 ± 2.09%, and47.95±7.86%, respectively. Samultang partially blocked PMA plus A23187-induced cyclooxygenase(COX)-2 expression. In addition, Samultang inhibited activation of nuclear factor (NF)-κB, andextracellular signal-regulated kinase (ERK) activation. These results suggest that anti-inflammatoryeffect of Samulatng may be mediated by the suppression of cytokine production and COX-2activation via down-regulation of NF-κB and ERK activation.