Curcumin is an in vivo inhibitor of angiogenesis.

  • Arbiser J
  • Klauber N
  • Rohan R
 et al. 
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BACKGROUND: Curcumin is a small-molecular-weight compound that is isolated from the commonly used spice turmeric. In animal models, curcumin and its derivatives have been shown to inhibit the progression of chemically induced colon and skin cancers. The genetic changes in carcinogenesis in these organs involve different genes, but curcumin is effective in preventing carcinogenesis in both organs. A possible explanation for this finding is that curcumin may inhibit angiogenesis.

MATERIALS AND METHODS: Curcumin was tested for its ability to inhibit the proliferation of primary endothelial cells in the presence and absence of basic fibroblast growth factor (bFGF), as well as its ability to inhibit proliferation of an immortalized endothelial cell line. Curcumin and its derivatives were subsequently tested for their ability to inhibit bFGF-induced corneal neovascularization in the mouse cornea. Finally, curcumin was tested for its ability to inhibit phorbol ester-stimulated vascular endothelial growth factor (VEGF) mRNA production.

RESULTS: Curcumin effectively inhibited endothelial cell proliferation in a dose-dependent manner. Curcumin and its derivatives demonstrated significant inhibition of bFGF-mediated corneal neovascularization in the mouse. Curcumin had no effect on phorbol ester-stimulated VEGF production.

CONCLUSIONS: These results indicate that curcumin has direct antiangiogenic activity in vitro and in vivo. The activity of curcumin in inhibiting carcinogenesis in diverse organs such as the skin and colon may be mediated in part through angiogenesis inhibition.

Author-supplied keywords

  • Angiogenesis Inhibitors
  • Angiogenesis Inhibitors: pharmacology
  • Animals
  • Antineoplastic Agents
  • Antineoplastic Agents: pharmacology
  • Cattle
  • Cell Differentiation
  • Cell Differentiation: drug effects
  • Cell Line, Transformed
  • Cell Line, Transformed: drug effects
  • Cell Line, Transformed: metabolism
  • Corneal Neovascularization
  • Corneal Neovascularization: chemically induced
  • Corneal Neovascularization: drug therapy
  • Curcumin
  • Curcumin: analogs & derivatives
  • Curcumin: pharmacology
  • Endothelial Growth Factors
  • Endothelial Growth Factors: genetics
  • Endothelial Growth Factors: metabolism
  • Endothelial Growth Factors: pharmacology
  • Endothelium, Vascular
  • Endothelium, Vascular: cytology
  • Endothelium, Vascular: drug effects
  • Enzyme Activation
  • Enzyme Activation: drug effects
  • Enzyme Inhibitors
  • Enzyme Inhibitors: pharmacology
  • Fibroblast Growth Factor 2
  • Fibroblast Growth Factor 2: pharmacology
  • Keratinocytes
  • Keratinocytes: drug effects
  • Keratinocytes: metabolism
  • Lymphokines
  • Lymphokines: genetics
  • Lymphokines: metabolism
  • Lymphokines: pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • NAD(P)H Dehydrogenase (Quinone)
  • NAD(P)H Dehydrogenase (Quinone): drug effects
  • NAD(P)H Dehydrogenase (Quinone): metabolism
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors

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  • J L Arbiser

  • N Klauber

  • R Rohan

  • R van Leeuwen

  • M T Huang

  • C Fisher

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