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苦蔘 에탄올 추출물이 NFκB 및 JNK, p38 조절을 통한 알레르기성 염증에 미치는 영향

The Effect of Allergic Inflamation by Sophora Flavescens Aiton Extract Ion Through Inhibition of the NFκB, JNK and p38 Pathway

박성식|이지영
사상체질면역의학회 (The Society of Sasang Constitution and Immune Medicine)|2009.04|사상체질면역의학회지 (Journal of Sasang Constitution and Immune Medicine)|제21권 제1호|pp. 139-149

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참고문헌

키워드

IL-6TNF-αIL-8Allergic InflammationSophora flavescens Aiton (SFA)MAPKs (JNKp38)NFκBrn
주제분류한의학

초록

1. Objectives The roots of Sophora flavescens Aiton (SFA) are widely used as a herbal remedy for allergic inflammation. In this study, we invested the effect of SFA on passive cutaneous anaphylaxis reaction and histamin releas and we demonstrated that SFA suppressed the production of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin- 6 (IL-6), and interleukin -8 (IL-8), through inhibition of the NFκB, JNK and p38 pathway in the human mast cell line, HMC-1. 2. Methods To accomplish this, we invested passive cutaneous anaphylaxis reaction and histamin release at an animal experiment. In addition, we investigated the effect of SFA on the production of inflammation-related cytokines in HMC-1 cells that were co-treated with PMA and A23187, which can induce production of pro-inflammatory cytokines. 3. Results and Conclusions SFA induced passive cutaneous anaphylaxis reaction and histamin releas and supressed the expression of TNF-α, IL-6, and IL-8. In addition, the protein levels of TNF-α were also decreased by SFA treatment. Furthermore, SFA inhibited the nuclear translocation of nuclear factor NFκB through inhibition of the phosphorylation and degradation of IκB-α, which is an inhibitor of NFκB. Moreover, SFA also inhibited induction of MAPKs (JNK, p38) and NFκB promoter-mediated luciferase activity. Taken together, these results suggest that SFA could be used as a treatment for mast cell-derived allergic inflammatory diseases.

Abstract

1. Objectives The roots of Sophora flavescens Aiton (SFA) are widely used as a herbal remedy for allergic inflammation. In this study, we invested the effect of SFA on passive cutaneous anaphylaxis reaction and histamin releas and we demonstrated that SFA suppressed the production of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin- 6 (IL-6), and interleukin -8 (IL-8), through inhibition of the NFκB, JNK and p38 pathway in the human mast cell line, HMC-1. 2. Methods To accomplish this, we invested passive cutaneous anaphylaxis reaction and histamin release at an animal experiment. In addition, we investigated the effect of SFA on the production of inflammation-related cytokines in HMC-1 cells that were co-treated with PMA and A23187, which can induce production of pro-inflammatory cytokines. 3. Results and Conclusions SFA induced passive cutaneous anaphylaxis reaction and histamin releas and supressed the expression of TNF-α, IL-6, and IL-8. In addition, the protein levels of TNF-α were also decreased by SFA treatment. Furthermore, SFA inhibited the nuclear translocation of nuclear factor NFκB through inhibition of the phosphorylation and degradation of IκB-α, which is an inhibitor of NFκB. Moreover, SFA also inhibited induction of MAPKs (JNK, p38) and NFκB promoter-mediated luciferase activity. Taken together, these results suggest that SFA could be used as a treatment for mast cell-derived allergic inflammatory diseases.

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