Journal
JOURNAL OF NEUROCHEMISTRY
Volume 105, Issue 2, Pages 557-564Publisher
WILEY
DOI: 10.1111/j.1471-4159.2007.05193.x
Keywords
astroglial cell; caffeic acid phenethyl ester; inflammation; JNK; NF-kappa B
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Caffeic acid phenethyl ester (CAPE), an active component of propolis extracts, has been known for its specific inhibition of nuclear factor kappa B (NF-kappa B) and subsequent anti-inflammatory activity. In this study, we report that (i) CAPE exerts its anti-inflammatory action (inhibition of tumor necrosis factor-induced expression of intercellular adhesion molecule-1 and CC chemokine ligand-2) via NF-kappa B inhibition by two distinct molecular mechanisms in a cell-specific manner: CAPE inhibited downstream pathways of inhibitor kappa B (I kappa B) degradation in monocytic cells, while activation of upstream I kappa B kinase was suppressed by CAPE pre-treatment in astroglial cells; and (ii) CAPE paradoxically activates the c-Jun N-terminal kinase (JNK) pathway, which might be responsible for its pro-apoptotic action and divergent regulation of proinflammatory mediators such as CXC chemokine ligand-8.
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