Inhibitory effect of citrus 5-hydroxy-3,6,7,8,3,4-hexamethoxyflavone on 12-O-tetradecanoylphorbol 13-acetate-induced skin inflammation and tumor promotion in mice
Identifieur interne : 002350 ( Main/Exploration ); précédent : 002349; suivant : 002351Inhibitory effect of citrus 5-hydroxy-3,6,7,8,3,4-hexamethoxyflavone on 12-O-tetradecanoylphorbol 13-acetate-induced skin inflammation and tumor promotion in mice
Auteurs : Ching-Shu Lai [Taïwan] ; Shiming Li [États-Unis] ; Chee-Yin Chai [Taïwan] ; Chih-Yu Lo [Taïwan] ; Chi-Tang Ho [États-Unis, Taïwan] ; Ying-Jan Wang [Taïwan] ; Min-Hsiung Pan [Taïwan]Source :
- Carcinogenesis [ 0143-3334 ] ; 2007-10-24.
Abstract
5-Hydroxy-3,6,7,8,3,4-hexamethoxyflavone (5-OH-HxMF), a polymethoxyflavone, is found exclusively in the Citrus genus, particularly in the peels of sweet orange. Herein, we report the first investigation of the inhibitory effects of 5-OH-HxMF on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in mouse skin. We found that the topical application of 5-OH-HxMF can effectively inhibit the transcriptional activation of iNOS and COX-2 mRNA and protein in mouse skin stimulated by TPA. Pre-treatment with 5-OH-HxMF resulted in the reduction of TPA-induced nuclear translocation of nuclear factor-B (NF-B) subunit and DNA binding by blocking phosphorylation of inhibitor B (IB) and p65 and subsequent degradation of IB. In addition, 5-OH-HxMF can inhibit TPA-induced phosphorylation and nuclear translocation of the signal transducer and activator of transcription-3. Moreover, 5-OH-HxMF can suppress TPA-induced activation of extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt, which are upstream of NF-B. We also found that 5-OH-HxMF significantly inhibited TPA-induced mouse skin inflammation by decreasing inflammatory parameters. Furthermore, 5-OH-HxMF significantly inhibited 7,12-dimethylbenz[a]anthracene/TPA-induced skin tumor formation by reducing the tumor incidence and tumor multiplicity of papillomas at 20 weeks. Therefore, all these results revealed for the first time that 5-OH-HxMF is an effective antitumor agent and its inhibitory effect is through the down-regulation of inflammatory iNOS and COX-2 gene expression in mouse skin, suggesting that 5-OH-HxMF is a novel functional agent capable of preventing inflammation-associated tumorigenesis.
Url:
DOI: 10.1093/carcin/bgm231
Affiliations:
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Herein, we report the first investigation of the inhibitory effects of 5-OH-HxMF on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in mouse skin. We found that the topical application of 5-OH-HxMF can effectively inhibit the transcriptional activation of iNOS and COX-2 mRNA and protein in mouse skin stimulated by TPA. Pre-treatment with 5-OH-HxMF resulted in the reduction of TPA-induced nuclear translocation of nuclear factor-B (NF-B) subunit and DNA binding by blocking phosphorylation of inhibitor B (IB) and p65 and subsequent degradation of IB. In addition, 5-OH-HxMF can inhibit TPA-induced phosphorylation and nuclear translocation of the signal transducer and activator of transcription-3. Moreover, 5-OH-HxMF can suppress TPA-induced activation of extracellular signal-regulated kinase 1/2, p38 mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt, which are upstream of NF-B. We also found that 5-OH-HxMF significantly inhibited TPA-induced mouse skin inflammation by decreasing inflammatory parameters. Furthermore, 5-OH-HxMF significantly inhibited 7,12-dimethylbenz[a]anthracene/TPA-induced skin tumor formation by reducing the tumor incidence and tumor multiplicity of papillomas at 20 weeks. Therefore, all these results revealed for the first time that 5-OH-HxMF is an effective antitumor agent and its inhibitory effect is through the down-regulation of inflammatory iNOS and COX-2 gene expression in mouse skin, suggesting that 5-OH-HxMF is a novel functional agent capable of preventing inflammation-associated tumorigenesis.</div></front></TEI><affiliations><list><country><li>Taïwan</li><li>États-Unis</li></country><region><li>New Jersey</li></region><settlement><li>New Brunswick (New Jersey)</li></settlement><orgName><li>Université Rutgers</li></orgName></list><tree><country name="Taïwan"><noRegion><name sortKey="Lai, Ching Shu" sort="Lai, Ching Shu" uniqKey="Lai C" first="Ching-Shu" last="Lai">Ching-Shu Lai</name></noRegion><name sortKey="Chai, Chee Yin" sort="Chai, Chee Yin" uniqKey="Chai C" first="Chee-Yin" last="Chai">Chee-Yin Chai</name><name sortKey="Ho, Chi Tang" sort="Ho, Chi Tang" uniqKey="Ho C" first="Chi-Tang" last="Ho">Chi-Tang Ho</name><name sortKey="Lai, Ching Shu" sort="Lai, Ching Shu" uniqKey="Lai C" first="Ching-Shu" last="Lai">Ching-Shu Lai</name><name sortKey="Lo, Chih Yu" sort="Lo, Chih Yu" uniqKey="Lo C" first="Chih-Yu" last="Lo">Chih-Yu Lo</name><name sortKey="Pan, Min Hsiung" sort="Pan, Min Hsiung" uniqKey="Pan M" first="Min-Hsiung" last="Pan">Min-Hsiung Pan</name><name sortKey="Pan, Min Hsiung" sort="Pan, Min Hsiung" uniqKey="Pan M" first="Min-Hsiung" last="Pan">Min-Hsiung Pan</name><name sortKey="Wang, Ying Jan" sort="Wang, Ying Jan" uniqKey="Wang Y" first="Ying-Jan" last="Wang">Ying-Jan Wang</name><name sortKey="Wang, Ying Jan" sort="Wang, Ying Jan" uniqKey="Wang Y" first="Ying-Jan" last="Wang">Ying-Jan Wang</name></country><country name="États-Unis"><region name="New Jersey"><name sortKey="Li, Shiming" sort="Li, Shiming" uniqKey="Li S" first="Shiming" last="Li">Shiming Li</name></region><name sortKey="Ho, Chi Tang" sort="Ho, Chi Tang" uniqKey="Ho C" first="Chi-Tang" last="Ho">Chi-Tang Ho</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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