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B, Activator Protein-1, and Apoptosis: Potential Role of Reactive Oxygen Intermediates and Lipid Peroxidation1
Cytokine Research Laboratory, Department of Bioimmunotherapy, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030
Resveratrol (trans-3,4',5-trihydroxystilbene), a
polyphenolic phytoalexin found in grapes, fruits, and root extracts of
the weed Polygonum cuspidatum, exhibits
anti-inflammatory, cell growth-modulatory, and anticarcinogenic
effects. How this chemical produces these effects is not known, but it
may work by suppressing NF-
B, a nuclear transcription factor that
regulates the expression of various genes involved in inflammation,
cytoprotection, and carcinogenesis. In this study, we investigated the
effect of resveratrol on NF-B activation induced by various
inflammatory agents. Resveratrol blocked TNF-induced activation of
NF-B in a dose- and time-dependent manner. Resveratrol also
suppressed TNF-induced phosphorylation and nuclear translocation of the
p65 subunit of NF-B, and NF-B-dependent reporter gene
transcription. Suppression of TNF-induced NF-B activation by
resveratrol was not restricted to myeloid cells (U-937); it was also
observed in lymphoid (Jurkat) and epithelial (HeLa and H4) cells.
Resveratrol also blocked NF-B activation induced by PMA, LPS,
H2O2, okadaic acid, and ceramide. The
suppression of NF-B coincided with suppression of AP-1. Resveratrol
also inhibited the TNF-induced activation of mitogen-activated protein
kinase kinase and c-Jun N-terminal kinase and abrogated TNF-induced
cytotoxicity and caspase activation. Both reactive oxygen intermediate
generation and lipid peroxidation induced by TNF were suppressed by
resveratrol. Resveratrol’s anticarcinogenic, anti-inflammatory,
and growth-modulatory effects may thus be partially ascribed to the
inhibition of activation of NF-B and AP-1 and the associated
kinases.
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