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Updated: Jan 22, 2026

Non-invasive Assessment of Microvascular and Endothelial Function
Published on: January 29, 2013
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.
Abstract:
The present study investigated the effects and mechanism by which curcumin suppresses intestinal microvascular endothelial cells (INMECs) invasion and angiogenesis induced by activated platelets. INMECs were obtained from healthy rats, and divided into five groups: Control, platelets, platelets +2.5 µM curcumin, platelets +5.0 µM curcumin and platelets +10.0 µM curcumin. Curcumin toxicity was determined and vascular endothelial growth factor (VEGF) concentrations of the five groups were measured using ELISA. The branch point numbers were measured using a capillary tube formation experiment, invasion cell numbers were evaluated with the Transwell assay, relative protein expression levels were measured with western blot assay and immunofluorescence staining of the nucleus. The 2.5, 5 and 10 µM curcumin concentrations were found to be suitable for INMECs. Curcumin significantly downregulated VEGF concentration, suppressed vascular lumen formation and inhibited invasion cell numbers in a dose-dependent manner. The α-smooth muscle actin, collagen I, E-cadherin, phosphorylated (p-) phosphoinositide 3-kinase (PI3K), p-protein kinase B (AKT), p-mammalian target of rapamycin (m-TOR) and hypoxia inducible factor subunit alpha (HIF-1α) protein expression levels of the curcumin-treated groups were significantly downregulated in a dose-dependent manner compared with the platelet group. HIF-1α protein expression levels in the nucleus of the curcumin-treated groups were significantly suppressed in a dose-dependent manner compared with the platelet group. In conclusion, curcumin suppressed INMEC invasion and angiogenesis induced by activated platelets via inhibiting the activation of the PI3K/AKT/mTOR pathway.
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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