ArticleFrontiers in pharmacology2026
Polysaccharide-rich birch sap attenuates kainic acid-induced acute seizures by suppressing TLR4/NF-κB-mediated inflammation and preserving blood-brain barrier and glutamate homeostasis.
Article in Frontiers in pharmacology, 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
Background: Plant polysaccharides possess significant anticonvulsant potential. This study investigated the neuroprotective effects of polysaccharide-rich birch sap (PRBS), previously characterized as primarily low-molecular-weight polysaccharides (MW·1.29 kDa), in a rat model of kainic acid (KA)-induced acute seizures. Methods: Rats received oral PRBS (6/10 mL/kg) for 7 days before KA-induced (15 mg/kg, i.p.) seizures. Seizure severity was evaluated using behavioral, electroencephalographic (EEG), and cerebral blood flow (CBF) monitoring. Brain tissues were analyzed via histology, Western blotting, and high-performance liquid chromatography (HPLC) for neuronal damage, neuroinflammation, blood-brain barrier (BBB) integrity, and glutamate metabolism. Results: Results demonstrated that the higher dose (10 mL/kg) exerted potent anticonvulsant effects, significantly reducing tonic convulsion scores and EEG ictal spikes. Furthermore, the treatment mitigated KA-induced CBF deficits and prevented neuronal damage in the cortex and hippocampus. Mechanistically, PRBS suppressed glial activation, indicated by a decrease in GFAP+ and OX42+ cells and reduced expression of markers associated with a pro-inflammatory state (C3 and CD86). It also inhibited neuroinflammatory signaling by downregulating TLR4 and p-IkB levels while suppressing the overall activation of NF-kB p65, thereby decreasing the release of pro-inflammatory cytokines (IL-1b, IL-6, and TNF-a). Additionally, the treatment attenuated BBB disruption by reducing albumin extravasation and upregulating tight junction proteins (claudin-5 and occludin). Finally, it restored glutamate homeostasis by upregulating the astrocytic transporter GLT-1 and glutamine synthetase, while downregulating glutamine transporters (SNAT1/3), glutaminase, and the vesicular glutamate transporter VGLUT1. Conclusion: PRBS exhibits potent antiseizure and neuroprotective properties that are closely associated with the modulation of TLR4/NF-kB-mediated inflammation, the preservation of BBB integrity, and the regulation of glutamate homeostasis, highlighting its potential as a natural therapeutic agent for seizures.
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