ArticleExperimental and therapeutic medicine2019
Curcumin suppresses intestinal microvascular endothelial cells invasion and angiogenesis induced by activated platelets.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Platelets and platelet-derived factors in curcumin treatment: a narrative review of mechanisms and translational potential.Open medicine (Warsaw, Poland) · 2026Review
- Angiogenesis as a Therapeutic Target of (Poly)phenols: Tackling Cancer and Vascular-Related Complications.Molecular nutrition & food research · 2025Review
- Targeting mTOR with curcumin: therapeutic implications for complex diseases.Inflammopharmacology · 2025Review
- Replacement in angiogenesis research: Studying mechanisms of blood vessel development by animal-freeFrontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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