Activation of NF-E2 p45-related factor-2 transcription and inhibition of intestinal tumor development by AHCC, a standardized extract of cultured <i>Lentinula edodes</i> mycelia

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  • Takahashi Maiko
    Division of Prevention, Center for Public Health Sciences, National Cancer Center
  • Fujii Gen
    Central Radioisotope Division, National Cancer Center
  • Hamoya Takahiro
    Division of Prevention, Center for Public Health Sciences, National Cancer Center
  • Kurokawa Yurie
    Division of Prevention, Center for Public Health Sciences, National Cancer Center
  • Matsuzawa Yui
    Division of Prevention, Center for Public Health Sciences, National Cancer Center
  • Miki Kohei
    Division of Prevention, Center for Public Health Sciences, National Cancer Center
  • Komiya Masami
    Division of Prevention, Center for Public Health Sciences, National Cancer Center
  • Narita Takumi
    Division of Prevention, Center for Public Health Sciences, National Cancer Center
  • Mutoh Michihiro
    Division of Prevention, Center for Public Health Sciences, National Cancer Center Division of Carcinogenesis and Cancer Prevention, National Cancer Center

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Abstract

<p>It has been reported that activation of NF-E2 p45-related factor-2 (NRF2), a transcription factor, induces a variety of antioxidant enzymes, and plays an important role in preventing carcinogenesis. AHCC is a standardized extract of cultured Lentinula edodes mycelia and it has been demonstrated to improve cancer. However, the effects of AHCC on NRF2 have not been examined, and the effects on intestinal adenoma development are not yet fully understood. We first investigated the effects of AHCC (1–5 mg/ml) on NRF2 activity in human colon cancer cell lines by a luciferase reporter gene assay, and found NRF2 transcriptional activities were increased ~12.6-fold. In addition, AHCC dose-dependently increased HO-1 and NQO-1 mRNA levels, and decreased interleukine-6 mRNA levels. Next, we administered 1,000 ppm AHCC for 8 weeks in the diet of Apc mutant Min mice, and found that AHCC significantly reduced the total number of intestinal polyps to 57.7% and to 67.6% of the control value in male and female Min mice, respectively, with suppression of interleukine-6 in the polyp part. These data suggest that AHCC possesses an ability to suppress cellular oxidative stress through activation of NRF2, thereby lowering intestinal polyp development in Min mice.</p>

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