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인간 비만세포에서 PMA와 A23187에 의해 유도된 전염증 매개체에 대한 신효월도산 추출물의 항염증 효과
위경 ( Gyeong Wi ),양다운 ( Da Wun Yang ),강옥화 ( Ok Hwa Kang ),김성배 ( Sung Bae Kim ),문수현 ( Su Hyun Mun ),서윤수 ( Yun Soo Seo ),강다혜 ( Da Hye Kang ),임재수 ( Jae Soo Lim ),김마룡 ( Ma Ryong Kim ),곽남원 ( Nam Won Kwak ) 대한본초학회 2014 大韓本草學會誌 Vol.29 No.6
Objectives : Sinhyowoldo-san (SHWDS) is said to be a traditional medicine used for shigellosis, abdominal pain, diarrhea. But mechanism of SHWDS mediated-modulation of immune function is not sufficiently understood. To ascertain the molecular mechanisms of SHWDS 70% EtOH extract on pharmacological and biochemical actions in inflammation, we researched the effect of pro-inflammatory mediators in phorbol-12-myristate-13-acetate (PMA)+ A23187-activated human mast cell line (HMC-1). Methods : In the present research, cell viability was measured by MTS assay. pro-inflammatory cytokine production was measured by performing enzyme-linked immunosorbent assay (ELISA), reverse transcription polymerase chain reaction (RT-PCR), and western blot analysis to analyze the activation of mitogen-activated protein kinases (MAPKs), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-кB). The investigation focused on whether SHWDS inhibited the expressions of interleukin-6 (IL-6), interleukin-8 (IL-8), MAPKs and NF-кB in PMA+A23187-activated HMC-1 cells. Results : SHWDS has no cytotoxicity at measured concentration (50, 100, and 250 μg/ml). SHWDS (250 μg/ml) inhibits pro-inflammatory cytokine expression in PMA+ A23187-activated HMC-1 cells. Moreover, SHWDS inhibited cyclooxygenase (COX)-2 expression. In activated HMC-1 cells, SHWDS suppressed phosphorylation of extracellular signal-regulated kinase (ERK 1/2) and c-jun N-terminal Kinase (JNK 1/2). Then, SHWDS suppressed activation of nuclear factor NF-кB in nuclear, degradation of IkB α in cytoplasm. Conclusions : We propose that SHWDS has an anti-inflammatory therapeutic potential, which may result from inhibition of ERK 1/2, JNK 1/2 phosphorylation and NF-кB activation, thereby decreasing the expression of pro-inflammatory genes.