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논문 기본 정보

자료유형
학술저널
저자정보
Soyoon Ryoo (Konkuk University) Jida Choi (Konkuk University) Jaemyung Kim (Animal and Plant Quarantine Agency) Suyoung Bae (Konkuk University) Jaewoo Hong (Konkuk University) Seunghyun Jo (Konkuk University) Soohyun Kim (Konkuk University) Youngmin Lee (Inje University)
저널정보
대한면역학회 Immune Network Immune Network Vol.13 No.6
발행연도
2013.12
수록면
283 - 288 (6page)

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초록· 키워드

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The pro-inflammatory cytokines tumor necrosis factor-α (TNFα) and interleukin (IL)-1β are crucial mediators involved in chronic inflammatory diseases. Inflammatory signal pathways regulate inflammatory cytokine expression-mediated by p38 mitogen activated protein kinase (p38MAPK). Therefore, considerable attention has been given to p38MAPK as a target molecule for the development of a novel anti-inflammatory therapeutics. BIRB 796, one of p38MAPK inhibitor, is a candidate of therapeutic drug for chronic inflammatory diseases. In this study, we investigated the effect of BIRB 796 on inflammatory cytokine productions by lipopolysaccharide (LPS) in different immune cell types. BIRB 796 reduced LPS-mediated IL-8 production in THP-1 cells but not in Raw 264.7 cells. Further analysis of signal molecules by western blot revealed that BIRB 796 sufficiently suppressed LPS-mediated phosphorylation of p38MAPK in both cell types whereas it failed to block inhibitor of kappa B (I-κB) degradation in Raw 264.7 cells. Taken together, these results suggest that the anti-inflammatory function of BIRB 796 depends on cell types.

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INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2016-511-001746028