ArticleCurrent medicinal chemistry2026
Betanin, a Natural Product from Red Beets, Improves Endothelial Dysfunction through Activation of Autophagy.
Article in Current medicinal chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveEndothelial dysfunction is the altered pathological ability of endothelial cells to modulate the passage of cells and solutes across vessels, which underlies the development of inflammatory diseases. Betanin (betanidin-5-O-β-glucoside), a natural product rich in red beets, is a water-soluble nitrogen-containing pigment, and its potential protective effects on cardiovascular disease have been reported. In this study, we investigated the protective role of betanin in vascular endothelial dysfunction induced by TNFα and explored potential mechanisms.
methodsWe modelled endothelial dysfunction through TNFα stimulation in human umbilical vein endothelial cells (HUVECs) and examined the role of betanin and its possible mechanism of action by MTT assay, Western blotting, and immunofluorescence staining. A systemic inflammation model of mice was built through LPS to investigate the protective roles of betanin.
resultsBetanin pre-treatment increased cell viability, inhibited the expression of intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM- 1), and improved endothelial tight junction by upregulating the expression of occludin and zonula occludens-1 (ZO-1) after TNFα stimulation in HUVECs. In terms of endothelial-mesenchymal transition, betanin up-regulated the expression of endothelial phenotypes VE-cadherin and CD31, whereas it inhibited the expression of mesenchymal phenotype N-cadherin, indicating that betanin reduced endothelial-mesenchymal transition in TNFα-stimulated HUVECs. In addition, betanin increased the expression of LC3 and decreased the expression of p62, two central proteins in autophagy. Betanin also reversed the abnormal autophagic flux after TNFα exposure. However, the specific autophagy inhibitor, 3-methyladenine, blocked the protective effect of betanin. Finally, betanin was found to greatly decrease ICAM-1 and VCAM-1 expression, and upregulate occludin and ZO-1 levels in a systemic inflammation model of mice.
conclusionThe above results collectively suggested that betanin may improve endothelial dysfunction by promoting autophagy, thus exerting beneficial effects on cardiovascular health.
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