Carcinogenesis, Vol 19, 1007-1012, Copyright © 1998 by Oxford University Press
T Ohata, K Fukuda, A Murakami, H Ohigashi, T Sugimura and K Wakabayashi
Although nitric oxide (NO) is an important biological mediator, excessive
production in inflammation is thought to be a causative factor of cellular
injury and cancer in the long term. In the present study the effects of
1'-acetoxychavicol acetate (ACA), which has anticarcinogenic properties, on
NO production in murine macrophage cell line RAW264 cells stimulated with
lipopolysaccharide or interferon- gamma were examined. ACA suppressed NO
production dose dependently with an IC50 of 160 ng/ml (680 nM). The
decrease in NO production was shown to parallel reduced expression of iNOS
mRNA and protein. The influence of ACA on transcription factors, such as
NF-kappaB, AP-1 and Stat1, which are involved in expression of the iNOS
gene was assessed. ACA was found to suppress degradation of IkappaB, an
NF-kappaB inhibitory factor, and consequently inhibit NF-kappaB activation.
Activation of AP- 1 and Stat1 was also blocked by ACA treatment. Thus we
demonstrate that ACA exerts potent inhibitory effects on NO production,
apparently mediated by modulation of activation of several transcription
factors. This could contribute to the anticarcinogenic properties of ACA.
ARTICLES
Inhibition by 1'-acetoxychavicol acetate of lipopolysaccharide- and interferon-gamma-induced nitric oxide production through suppression of inducible nitric oxide synthase gene expression in RAW264 cells
Cancer Prevention Division, National Cancer Center Research Institute, Tokyo, Japan.
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