Sang-Yong Kim

Anti-Allergic Effects of Artemisia iwayomogi on Mast Cell–Mediated Allergy Model

The discovery of drugs for the treatment of allergic disease is an important subject in human health. The Artemisia iwayomogi (Compositae) (AIE) has been used as a traditional medicine in Korea and is known to have an anti-inflammatory effect. However, its specific mechanism of action is still unknown. In this report, we investigated the effect of AIE on the mast cell-mediated allergy model and studied the possible mechanism of action. AIE inhibited compound 48/80–induced systemic reactions and plasma histamine release in mice. AIE decreased immunoglobulin E (lgE)–mediated local allergic reaction, passive cutaneous anaphylaxis (PCA) reaction. AIE dose dependency attenuated histamine release from rat peritoneal mast cells activated by compound 48/80 or IgE. AIE decreased the compound 48/80-induced intracellular Ca2+. Furthermore, AIE decreased the phorbol 12-myristate 13-acetate (PMA) plus calcium lonophore A23187-stimulated tumor necrosis factor-α and interleukin-6 gene expression and production in human mast cells. The inhibitory effect of AIE on the proinflammatory cytokine was p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) dependent. AIE attenuated PMA plus A23187-lnduced degradation of licBa and nuclear translocation of NF-κB and specifically blocked activation of p38 MAPK but not that of c-jun N-terminal kinase and extracellular signal-regulated kinase. Our findings provide evidence that AIE inhibits mast cell-derived immediate-type allergic reactions and involvement of Intracellular Ca2+, proinflammatory cytokines, p38 MAPK, and NF-κB in these effects.

Epigallocatechin-3-Gallate Inhibits Secretion of TNF-α, IL-6 and IL-8 through the Attenuation of ERK and NF-κB in HMC-1 Cells

Background: Epigallocatechin-3-gallate (EGCG) is a major form of tea catechin and has a variety of biological activities. In the present study, we investigated the effect of EGCG on the secretion of TNF-α, IL-6 and IL-8, as well as its possible mechanism of action by using the human mast cell line (HMC-1). Methods: EGCG was treated before the activation of HMC-1 cells with phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore (A23187). To investigate the effect of EGCG on PMA+A23187-stimulated HMC-1 cells, ELISA, Western blot analysis, electrophorectic mobility shift assay and luciferase assay were used in this study. Results: EGCG (100 µM) inhibited PMA+A23187-induced TNF-α, IL-6 and IL-8 expression and production. EGCG inhibited the intracellular Ca2+ level. EGCG attenuated PMA+A23187-induced NF-ĸB and extracellular signal-regulated kinase (ERK1/2) activation, but not that of c-Jun N-terminal kinase or p38 mitogen-activated protein kinase. Conclusion: EGCG inhibited the production of TNF-α, IL-6 and IL-8 through the inhibition of the intracellular Ca2+ level, and of ERK1/2 and NF-ĸB activation. These results indicate that EGCG may be helpful in regulating mast-cell-mediated allergic inflammatory response.

Effects of Prunella vulgaris on Mast Cell–Mediated Allergic Reaction and Inflammatory Cytokine Production

In this study, we investigated the effect of aqueous extract of Prunella vulgaris (Labiatae; PVAE) on the mast cell–mediated allergy model. We found that PVAE (0.001–0.1 g/kg) dose dependently inhibited compound 48/80–induced systemic anaphylaxis and serum histamine release in mice. PVAE decreased the IgE-mediated local allergic reaction, passive cutaneous anaphylaxis. In addition, PVAE attenuated phorbol 12-myristate 13-acetate (PMA) and calcium ionophore A23187-stimulated TNF-α, IL-6, and IL-8 secretion in human mast cells. The inhibitory effect of PVAE on proinflammatory cytokines was nuclear factor-κB (NF-κB) dependent. PVAE suppressed PMA and A23187-induced NF-κB/DNA binding activity and NF-κB–dependent gene reporter assay. Our findings provide evidence that PVAE inhibits mast cell–derived immediate-type allergic reactions and involvement of proinflammatory cytokines and NF-κB in these effects.

Anti-inflammatory activity of Motherwort (Leonurus sibiricus L.).

Motherwort (MW), a Korean folk medicine, has been applied to treat inflammatory disease. However, its effect on inflammatory cytokine release from mast cells is not well known. We investigated the anti- inflammatory effect of MW on the secretion of inflammatory cytokine such as tumor necrosis factor (TNF)-α and interleukin (IL)-6 and IL-8 in human mast cell line (HMC-1). MW was treated in vitro before activation of HMC-1 cells with phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187. MW had no cytotoxic effects on HMC-1 cell viability. MW (1 mg/ml) inhibited PMA plus A23187-stimulated gene expression and production of TNF-α, IL-6, and IL-8. Stimulation with PMA plus A23187 induced NF-κB activation in HMC-1 cells, which was inhibited by MW (1 mg/ml). MW inhibited secretion of TNF-α, IL-6, and IL-8 possibly by inhibiting NF-κB activation. These results indicate that MW may be helpful in regulating inflammatory diseases.

Isodon japonicus Inhibits Mast Cell‐Mediated Immediate‐Type Allergic Reactions

The effect of aqueous extract of Isodon japonicus Hara (Labiatae) (IJAE) on mast cell‐mediated immediate‐type allergic reactions was investigated. IJAE inhibited systemic allergic reaction induced by compound 48/80. When IJAE was pretreated at the same concentrations with systemic allergic reaction test, the plasma histamine levels were reduced in a dose‐dependent manner. IJAE also inhibited local allergic reaction activated by anti‐dinitrophenyl (DNP) IgE antibody. IJAE dose‐dependently inhibited the histamine release from rat peritoneal mast cells (RPMC) activated by compound 48/80 or anti‐DNP IgE. IJAE inhibited the secretion of tumor necrosis factor‐α (TNF‐α) and interleukin (IL)‐6 in phorbol 12‐myristate 13‐acetate (PMA) plus calcium ionophore A23187‐stimulated human mast cell line (HMC‐1) cells. In addition, the expression of TNF‐α mRNA in HMC‐1 cells was inhibited by IJAE. These results indicate that IJAE may be beneficial in the regulation of immediate‐type allergic reaction.

The effect of Jeo Dang-Tang on cytokines production in the patients with cerebral infarction

Abstract The herbal formulation “Jeo Dang‐Tang” (JDT) has long been used for various cerebrovascular diseases. However, very little has scientific investigation been carried out. The aim of the present study is to investigate the effect of JDT on the production of various cytokines in the patients with cerebral infarction (CI). Peripheral blood mononuclear cells (PBMC) obtained from the patients with CI were cultured for 24 h in the presence or absence of lipopolysaccharide (LPS) or phytohemagglutinin (PHA). The amount of interleukin (IL)‐4, IL‐10 and transforming growth factor (TGF)‐1β, in culture supernatant, was significantly increased in the JDT, LPS or PHA treated cells compared to unstimulated cells (P < 0.05). We also show that increased IL‐4, and IL‐10 level by LPS or PHA was significantly inhibited by JDT in a dose‐dependent manner. Maximal inhibition rate of IL‐4 and IL‐10 production by JDT was 45 ± 2% and 51 ± 5% for LPS‐stimulated cell and 41.5 ± 3% and 70.8 ± 2% for PHA‐stimulated cells, respectively (P < 0.05). On the other hand, JDT significantly increased the LPS or PHA‐induced TGF‐β1 production (P < 0.05). These data suggest that JDT has a regulatory effect on the cytokines production, which might explain its beneficial effect in the treatment of CI.