A newly synthesized compound, 4′‐geranyloxyferulic acid–<i>N</i>(omega)‐nitro‐<scp>l</scp>‐arginine methyl ester suppresses inflammation‐associated colorectal carcinogenesis in male mice

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  • Masahito Shimizu
    Department of Internal Medicine/Gastroenterology Gifu University Graduate School of Medicine Gifu Japan
  • Takahiro Kochi
    Department of Internal Medicine/Gastroenterology Gifu University Graduate School of Medicine Gifu Japan
  • Yohei Shirakami
    Department of Internal Medicine/Gastroenterology Gifu University Graduate School of Medicine Gifu Japan
  • Salvatore Genovese
    Dipartimento di Farmacia Università ‘G. D'Annunzio’ Chieti‐Pescara Chieti Scalo (CH) Italy
  • Francesco Epifano
    Dipartimento di Farmacia Università ‘G. D'Annunzio’ Chieti‐Pescara Chieti Scalo (CH) Italy
  • Serena Fiorito
    Dipartimento di Farmacia Università ‘G. D'Annunzio’ Chieti‐Pescara Chieti Scalo (CH) Italy
  • Takayuki Mori
    Department of Pharmacy Ogaki Municipal Hospital Ogaki Japan
  • Takuji Tanaka
    Department of Tumor Pathology Gifu University Graduate School of Medicine Gifu Japan
  • Hisataka Moriwaki
    Department of Internal Medicine/Gastroenterology Gifu University Graduate School of Medicine Gifu Japan

書誌事項

公開日
2014-01-28
資源種別
journal article
権利情報
  • http://onlinelibrary.wiley.com/termsAndConditions#vor
DOI
  • 10.1002/ijc.28718
公開者
Wiley

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説明

<jats:p>We previously reported the cancer chemopreventive activity of 4′‐geranyloxyferulic acid (GOFA, Miyamoto et al., Nutr Cancer 2008; 60:675‐84) and a β‐cyclodextrin inclusion compound of GOFA (Tanaka et al., Int J Cancer 2010; 126:830‐40) in colitis‐related colorectal carcinogenesis. In our study, the chemopreventive effects of a newly synthesized GOFA‐containing compound, GOFA–<jats:italic>N</jats:italic>(omega)‐nitro‐<jats:sc>l</jats:sc>‐arginine methyl ester (L‐NAME), which inhibits inducible nitric oxide (iNOS) and cyclooxygenase‐2 (COX) enzymes, were investigated using a colitis‐associated mouse colorectal carcinogenesis model with azoxymethane (AOM) and dextran sodium sulfate (DSS). The dietary administration of GOFA–L‐NAME after the AOM and DSS treatments significantly reduced the multiplicity of adenocarcinomas (inhibition rates: 100 ppm, 84%, <jats:italic>p</jats:italic> < 0.001; 500 ppm, 94%, <jats:italic>p</jats:italic> < 0.001) compared with the AOM + DSS group. Dietary GOFA–L‐NAME significantly decreased the proliferation (<jats:italic>p</jats:italic> < 0.001) and increased the apoptosis (<jats:italic>p</jats:italic> < 0.001) of colonic adenocarcinoma cells. A subsequent short‐term experiment revealed that dietary GOFA–L‐NAME decreased the mRNA expression of inflammatory enzymes, such as iNOS and COX‐2, and proinflammatory cytokines, such as tumor necrosis factor‐α, interleukin (IL)−1β, IL‐6 and macrophage inflammatory protein (MIP)−2 in the colonic mucosa of mice that received 1.5% DSS in their drinking water for 7 days. Our findings indicate that GOFA–L‐NAME is able to inhibit colitis‐associated colon carcinogenesis by modulating inflammation, proliferation, apoptosis and the expression of proinflammatory cytokines in mice.</jats:p>

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