RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      검색결과 좁혀 보기

      선택해제

      오늘 본 자료

      • 오늘 본 자료가 없습니다.
      더보기
      • 무료
      • 기관 내 무료
      • 유료
      • KCI등재

        Sulforaphane Inhibits TNF-α-Induced Adhesion Molecule Expression Through the Rho A/ROCK/NF-κB Signaling Pathway

        Chi-Nan Hung,Hui-Pei Huang,Chau-Jong Wang,Kai-Li Liu,Chong-Kuei Lii 한국식품영양과학회 2014 Journal of medicinal food Vol.17 No.10

        Endothelial dysfunction is an early indicator of cardiovascular diseases. Increased stimulation of tumor necrosis factor-a (TNF-a) triggers the inflammatory mediator secretion of endothelial cells, leading to atherosclerotic risk. In this study, we investigated whether sulforaphane (SFN) affected the expression of intracellular adhesion molecule-1 (ICAM-1) in TNF-a-induced ECV 304 endothelial cells. Our data showed that SFN attenuated TNF-a-induced expression of ICAM-1 in ECV 304 cells. Pretreatment of ECV 304 cells with SFN inhibited dose-dependently the secretion of proinflammatory cytokines, such as interleukin (IL)-1b, IL-6, and IL-8. SFN inhibited TNF-a-induced nuclear factor-jB (NF-jB) DNA binding activity. Furthermore, SFN decreased TNF-a-mediated phosphorylation of IjB kinase (IKK) and IjBa, Rho A, ROCK, ERK1/2, and plasminogen activator inhibitor-1 (PAI-1) levels. Collectively, SFN inhibited the NF-jB DNA binding activity and downregulated the TNF-a-mediated induction of ICAM-1 in endothelial cells by inhibiting the Rho A/ROCK/NF-jB signaling pathway, suggesting the beneficial effects of SFN on suppression of inflammation within the atherosclerotic lesion.

      연관 검색어 추천

      이 검색어로 많이 본 자료

      활용도 높은 자료

      해외이동버튼