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Involvement of NF-${kappa}B$ in the Inhibitory Actions of Platycarya strobilacea on the TNF-$alpha$-Induced Monocyte Adhesion to Colon Epithelial Cells and Chemokine Expression
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  • Involvement of NF-${kappa}B$ in the Inhibitory Actions of Platycarya strobilacea on the TNF-$alpha$-Induced Monocyte Adhesion to Colon Epithelial Cells and Chemokine Expression
  • Involvement of NF-${kappa}B$ in the Inhibitory Actions of Platycarya strobilacea on the TNF-$alpha$-Induced Monocyte Adhesion to Colon Epithelial Cells and Chemokine Expression
저자명
Babu. Dinesh,Lee. Jong-Suk,Park. Su-Young,Thapa. Dinesh,Choi. Mi-Kyoung,Kim. Ah-Ra,Park. Young-Joon,Kim. Jung-Ae
간행물명
Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea
권/호정보
2008년|31권 6호|pp.727-735 (9 pages)
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대한약학회
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정기간행물|ENG|
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
서지반출

기타언어초록

Oxidative stress and the activation of nuclear factor (NF)-${kappa}B$ play crucial roles in the pathogenesis of inflammatory bowel disease (IBD). In the present study, we examined the effects of the ethanol extract of Platycarya strobilacea Sieb. stem (EPS) on TNF-$alpha$-induced monocyte adhesion to HT29 human colon epithelial cells, an initial step of colon inflammation. EPS contained high amount of polyphenols ($0.241{pm}0.017;mg$ of catechin equivalent/g of extract) and showed substantial DPPH radical scavenging activity. In addition, EPS significantly suppressed TNF-$alpha$-induced reactive oxygen species (ROS) increase. Moreover, TNF-$alpha$-induced monocyte adhesion to HT29 colon epithelial cells was significantly suppressed by EPS in a concentrationdependent manner. The reduced adhesion by EPS was correlated with suppressed expression of MCP-1 and IL-8, the major chemokines in IBD. EPS also prevented the TNF-$alpha$-induced nuclear translocation of NF-${kappa}B$, one of the redox-sensitive transcription factors, in a concentration-dependent manner. Taken together, our results suggest that the anti-oxidant components of EPS prevent TNF-$alpha$-induced NF-${kappa}B$ activation, chemokine induction, and monocyte adhesion at the site of intestinal inflammation.