ArticleJournal of neuroinflammation2025
Tubuloside B ameliorates blood-brain barrier disruption and cognitive deficits after cerebral ischemia by inhibiting TRIC protein ubiquitination and degradation.
Article in Journal of neuroinflammation, 2025. 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
background and purposeVascular cognitive impairment (VCI) is strongly linked to blood-brain barrier (BBB) dysfunction. This study investigated whether Tubuloside B (Tub-B), a primary bioactive compound of Cistanche tubulosa, ameliorates cognitive deficits by protecting BBB integrity through inhibition of tricellulin (TRIC) ubiquitination and degradation.
methodsThe main plasma metabolites of total glycosides of Cistanche (TCGs) were identified by UPLC-QQQ-MS. A bilateral common carotid artery occlusion (BCCAO) rat model was used to induce chronic cerebral hypoperfusion (CCH). Cognitive function was assessed using the Morris water maze, and BBB permeability was evaluated by Evans blue extravasation. The concentrations of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-10, and transforming growth factor-β (TGF-β), in the rat hippocampal tissues were quantified using ELISA kits. TRIC expression and ubiquitination were analyzed by Western blot, co-immunoprecipitation, and immunohistochemistry. An in vitro oxygen-glucose deprivation (OGD) model in brain microvascular endothelial cells was used to validate the effects on barrier function.
resultsTub-B was identified as the major circulating metabolite, accounting for 52.3% ± 2.1% of plasma components. In CCH rats, Tub-B (20 mg/kg) significantly improved spatial memory, increasing platform crossings (3.00 ± 0.58 vs. CCH, P < 0.05) and reducing Evans blue leakage (0.038 ± 0.007 µg/g tissue vs. 0.15 ± 0.02 µg/g in CCH, P < 0.001). Furthermore, Tub-B treatment dose-dependently suppressed pro-inflammatory cytokines (TNF-α, IL-1β) and concomitantly enhanced anti-inflammatory cytokines (IL-10, TGF-β) in the hippocampus. It also attenuated the downregulation of TRIC and suppressed its ubiquitination. In OGD-injured endothelial cells, Tub-B enhanced barrier integrity and inhibited TRIC ubiquitination.
conclusionTub-B attenuates CCH-induced BBB disruption and cognitive impairment by inhibiting TRIC ubiquitination and degradation, likely via interference with VEGF signaling. These results highlight its potential as a therapeutic agent for VCI.
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