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Differential regulation of c‐Jun N‐terminal kinase and NF‐κB pathway by caffeic acid phenethyl ester in astroglial and monocytic cells
Author(s) -
Choi Kyungsun,
Choi Chulhee
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.05193.x
Subject(s) - caffeic acid phenethyl ester , microbiology and biotechnology , kinase , nf κb , proinflammatory cytokine , chemistry , tumor necrosis factor alpha , chemokine , c jun , signal transduction , biology , biochemistry , inflammation , caffeic acid , receptor , immunology , transcription factor , antioxidant , gene
Caffeic acid phenethyl ester (CAPE), an active component of propolis extracts, has been known for its specific inhibition of nuclear factor κB (NF‐κB) 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‐κB inhibition by two distinct molecular mechanisms in a cell‐specific manner: CAPE inhibited downstream pathways of inhibitor κB (IκB) degradation in monocytic cells, while activation of upstream IκB 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.