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Antiangiogenic effect of alpha-anordrin in vitro and in vivo

Z C Ma1, L G Lou, Z Zhang

  • 1Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 200031, China.

Acta Pharmacologica Sinica
|August 15, 2001
PubMed
Abstract

Insights

Alpha-anordrin (alpha-Ano) exhibits antiangiogenic properties by inhibiting endothelial cell proliferation and migration. This effect is linked to reduced nitric oxide (NO) levels, independent of estrogen receptor activity.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Oncology

Background:

  • Angiogenesis is crucial for tumor growth and metastasis.
  • Estrogen receptor (ER) signaling plays a role in angiogenesis.
  • Alpha-anordrin (alpha-Ano) is investigated as a potential antiangiogenic agent.

Purpose of the Study:

  • To evaluate the antiangiogenic effect of alpha-anordrin (alpha-Ano).
  • To determine the mechanism underlying alpha-Ano's antiangiogenic action, including its relation to nitric oxide (NO) and estrogen receptor (ER) pathways.

Main Methods:

  • In vivo studies using microvascular density (MVD) in Lewis lung carcinoma and the chicken chorioallantoic membrane (CAM) model.
  • In vitro assessment of human umbilical vein endothelial cell (HUVEC) proliferation, migration, and attachment.
  • Measurement of nitric oxide (NO) levels in HUVECs.

Main Results:

  • Alpha-Ano significantly inhibited MVD and tumor growth in vivo.
  • Alpha-Ano demonstrated antiangiogenic effects in the CAM model (53% inhibition), unaffected by 17 beta-estradiol.
  • In vitro, alpha-Ano suppressed HUVEC proliferation and migration but not attachment, while dose-dependently reducing NO levels.

Conclusions:

  • Alpha-anordrin possesses significant antiangiogenic activity.
  • The antiangiogenic effect of alpha-Ano is mediated by the reduction of nitric oxide (NO) levels.
  • Alpha-Ano inhibits endothelial cell proliferation and migration, independent of estrogen receptor signaling.

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