Curcumin suppresses intestinal microvascular endothelial cells invasion and angiogenesis induced by activated

Su Xu1, Zhao-Xiu Xu2, Shuai Yan3

  • 1Department of Anorectal Surgery, Yancheng Hospital of Traditional Chinese Medicine Affiliated to Nanjing University of Chinese Medicine, Yancheng, Jiangsu 224001, P.R. China.

Insights

Curcumin effectively inhibits intestinal microvascular endothelial cell invasion and angiogenesis triggered by activated platelets. This natural compound works by downregulating vascular endothelial growth factor (VEGF) and blocking the PI3K/AKT/mTOR signaling pathway.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Platelet activation plays a role in intestinal microvascular endothelial cell (INMEC) invasion and angiogenesis.
  • Curcumin, a compound found in turmeric, has demonstrated anti-inflammatory and anti-angiogenic properties.

Purpose of the Study:

  • To investigate the inhibitory effects of curcumin on INMEC invasion and angiogenesis induced by activated platelets.
  • To elucidate the underlying molecular mechanisms of curcumin's action.

Main Methods:

  • INMECs were treated with varying concentrations of curcumin in the presence of activated platelets.
  • Vascular endothelial growth factor (VEGF) levels were measured using ELISA.
  • Capillary tube formation, cell invasion, and protein expression (Western blot, immunofluorescence) were assessed.

Main Results:

  • Curcumin (2.5–10 µM) was not toxic to INMECs and significantly reduced VEGF levels.
  • Curcumin dose-dependently suppressed vascular lumen formation and INMEC invasion.
  • Curcumin downregulated key proteins in the PI3K/AKT/mTOR pathway and HIF-1α expression.

Conclusions:

  • Curcumin effectively suppresses platelet-induced INMEC invasion and angiogenesis.
  • The mechanism involves the inhibition of the PI3K/AKT/mTOR signaling pathway and reduced HIF-1α expression.

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