ePoster

HYDROXYTYROSOL PRESERVES NEUROVASCULAR PROPERTIES UNDER LPS-INDUCED INFLAMMATION

Daniela M. Simõesand 3 co-authors

University of Coimbra

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-065

Presentation

Date TBA

Board: PS05-09AM-065

Poster preview

HYDROXYTYROSOL PRESERVES NEUROVASCULAR PROPERTIES UNDER LPS-INDUCED INFLAMMATION poster preview

Event Information

Poster Board

PS05-09AM-065

Abstract

Mediterranean diet (MedDiet) has been associated with a wide range of health benefits and includes a high intake of olive oil, which contains polyphenols such as hydroxytyrosol (HT). We investigate the modulation of BBB by HT. To address this issue, an in vitro BBB model was exposed to HT (50μM) with or without lipopolysaccharide (LPS; 50μg/mL). Functional barrier integrity was assessed by transendothelial electrical resistance (TEER) and paracellular and transcellular transport. Endothelial and inflammatory markers were assessed by western blot, immunocytochemistry, qPCR and ELISA. LPS disrupted BBB function by decreasing TEER and increasing endothelial permeability. These functional changes were associated with reduced gene expression of tight junction components (TJP1 and OCLN) and decreased protein levels of occludin and β-catenin, as well as increased PLVAP gene expression. Also, LPS upregulated the gene expression of adhesion molecules (VCAM, ICAM1, EDN1), increased ICAM-1 protein levels, and elevated pro-inflammatory mediators (IL6, IL1B genes and TNF-α protein), promoting monocyte migration. HT significantly restored barrier function, as shown by increased TEER and reduced endothelial permeability. This functional protection was accompanied by upregulation of TJP1 gene and increased β-catenin protein levels. Importantly, HT attenuated inflammatory mediators by downregulating IL6, IL1B, EDN1 and ICAM1, as well as by decreasing ICAM-1 and TNF-α protein levels. Overall, these findings indicate that HT preserves BBB homeostasis and supports its potential as a dietary intervention to counteract inflammatory-associated neurovascular dysfunction and neuroinflammation.
Supported by "CHAngeing, Excellence Hubs" funded by the European Union's HORIZON-WIDERA-2022-ACCESS-04-01 and FCT: UID/04539/2025 (CiBB).

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