Specific Inhibition of Hypoxia-inducible Factor (HIF)-1α Activation and of Vascular Endothelial Growth Factor (VEGF) Production by Flavonoids

  • Hasebe Yuki
    Department of Microbiology, Showa University of Pharmaceutical Sciences
  • Egawa Kiyoshi
    Department of Microbiology, Showa University of Pharmaceutical Sciences
  • Yamazaki Yoko
    Institute of Microbial Chemistry, Tokyo
  • Kunimoto Setsuko
    Institute of Microbial Chemistry, Tokyo
  • Hirai Yasuaki
    Department of Pharmacognosy and Phytochemistry, Showa University of Pharmaceutical Sciences
  • Ida Yoshiteru
    Department of Pharmacognosy and Phytochemistry, Showa University of Pharmaceutical Sciences
  • Nose Kiyoshi
    Department of Microbiology, Showa University of Pharmaceutical Sciences

書誌事項

タイトル別名
  • Specific Inhibition of Hypoxia-inducible Factor (HIF)-1.ALPHA. Activation and of Vascular Endothelial Growth Factor (VEGF) Production by Flavonoids
  • Specific Inhibition of Hypoxia inducible Factor HIF 1 アルファ Activation and of Vascular Endothelial Growth Factor VEGF Production by Flavonoids

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抄録

Screening using a reporter under the control of the hypoxia-response element (HRE) identified several flavonoids and homoisoflavonoids that inhibit the activation of HRE under hypoxic conditions. Among various compounds, isorhamnetin, luteolin, quercetin, and methyl ophiopogonanone B (MOB) were effective at 3 to 9 μg/ml in inhibiting the reporter activity. The expression of vascular endothelial growth factor (VEGF) mRNA during hypoxia was also inhibited by MOB in HepG2 cells, but the effective doses were 10 to 20 μg/ml. MOB caused destabilization of hypoxia-inducible factor (HIF)-1α, as revealed by Western blotting, that was dependent on proteasome activity and the tumor suppressor, p53. The tubular formation and migration of human umbilical vein endothelial cells was also inhibited by MOB. MOB is expected to act as an inhibitor of angiogenesis.

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