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CIRCULATING EXTRACELLULAR VESICLES FROM LIVER INJURY DRIVE NEUROINFLAMMATION IN THE HIPPOCAMPUS
Reza Azadnasaband 2 co-authors
Centro de Investigación Principe Felipe
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS04-08PM-052
Presentation
Date TBA
Board: PS04-08PM-052
Event Information
Poster Board
PS04-08PM-052
Poster
View posterAbstract
Neuroinflammation is present in the hippocampus of patients and animal models with hepatic encephalopathy (HE), even at mild stages, and contributes to cognitive impairment. This study aimed to determine whether extracellular vesicles (EVs) from plasma of rats with liver damage contribute to hippocampal neuroinflammation and whether rifaximin, a non-absorbable antibiotic used in HE treatment, can modify EV cargo to prevent these effects. Liver damage was induced in male rats by carbon tetrachloride (CCl₄). EVs were isolated from plasma of rats treated with vehicle, rifaximin, CCl₄, or CCl₄ + rifaximin after 4 weeks (mild damage) or 12 weeks (severe damage). Hippocampal slices from healthy rats were incubated with these EV groups. Neuroinflammatory markers were quantified by Western blot, and microglial and astrocytic activation were evaluated by immunohistochemistry and immunofluorescence. EVs from 4-week CCl₄-treated rats induced increased pro-inflammatory factors such as TNF-α in microglial cells and IL-1β. EVs from 12-week CCl₄-treated rats additionally triggered strong microglia and astrocyte activation and increased HMGB1 and CCL2. In contrast, EVs from CCl₄ + rifaximin-treated rats showed a markedly reduced ability to induce neuroinflammation, as they did not activate glial cells or elevate TNF-α, IL-1β or HMGB1. These findings indicate that circulating EVs contribute to hippocampal neuroinflammation associated with liver damage, and that rifaximin modifies EV cargo in a way that attenuates CCl₄-induced neuroinflammatory responses.
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