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Intestinal Research 2005;3(1):38-47.
Published online June 30, 2005.
The Effect of DA-6034, a Synthetic Derivative of Flavonoid, on NF-κB Activity Stimulated with Lipopolysaccharide and Tumor Necrosis actor-α in Human Colonic Epithelial Cell Line
Ji Won Kim, Yong-Jin Jung, Ji Bong Jeong, Byeong Gwan Kim, Kook Lae Lee, Joo Sung Kim, Hyun Chae Jung, In Sung Song
Department of Internal Medicine, Seoul National University Boramae Hospital, Department of Internal Medicine, College of Medicine, Seoul National University, Seoul, Korea
플라보노이드 합성 유도체인 DA-6034가 인간 대장 점막 상피 세포주에서 Lipopolysaccharide 및 Tumor Necrosis Factor-α 자극에 의한 NF-κB의 활성화에 미치는 영향
김지원, 정용진, 정지봉, 김병관, 이국래, 김주성, 정현채, 송인성
서울대학교 보라매병원, 서울대학교 의과대학 내과학교실
The nuclear factor-κB (NF-κB) is associated with expression of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8). DA-6034, a derivative of flavonoid, has shown a potent anti-inflammatory effect in IBD animal model. The aim of this study was to characterize the anti-inflammatory activity of DA-6034 in terms of regulation of NF-κB. Methods: HT-29 cells were stimulated with lipopolysaccharide (LPS) or TNF-α alone or pretreated with DA-6034. The influence of DA-6034 on NF-κB DNA binding activity and inhibitory protein κB (IκB) activity was determined using an electrophoretic mobility shift assay (EMSA) and Western blot analysis. The RT-PCR method was used to determine the degree of gene expression of TNF-α and IL-8. Production of TNF-α and IL-8 protein was measured by ELISA. Results: DA-6034 prevented NF-κB activation stimulated with LPS and TNF-α and inhibited LPS- and TNF-α-induced IκB degradation. LPS-induced TNF-α mRNA expression and TNF-α-induced IL-8 mRNA expression were significantly decreased by DA-6034 pretreatment as compared to the absence of DA-6034 pretreatment. Conclusions: These results suggest that the inhibitory effect of DA-6034 on the production of TNF-α in LPS-stimulated and IL-8 in TNF-α-stimulated HT-29 cells may involve transcription regulation by suppression of NF-κB activation by interfering with IκB degradation. (Intest Res 2005; 3:38-47)
Key Words: IBD, DA-6034, NF-κB, IκB
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