β-glucan-loaded nano-niosomes ameliorate spatial and associative memory impairment in a D-galactose-induced aging rat model via modulation of microglial pyroptosis and autophagy - 07/01/26
, Soheila Adeli c, Hamidreza Sahrayi d, Seyed Morteza Karimian e, f, ⁎ Abstract |
Introduction |
Considering the anti-inflammatory effects of β-glucan, a natural polysaccharide, this study investigated whether β-glucan nano-formulated in niosomes (vesicles made of non-ionic surfactants used for drug delivery) could improve spatial and associative memories in a D -galactose-induced aging rat model by modulating neuroinflammation, microglial autophagy (cellular recycling by microglia), and pyroptosis (inflammatory programmed cell death).
Methods |
Sixty Wistar rats were randomly divided into six groups ( n = 10 pre group). An aging model was induced in relevant groups via chronic D -galactose injection (180 mg/kg, i.p.) for 8 weeks. Anti-inflammatory effects of orally administered β-glucan (8 mg/kg) encapsulated in nano-niosomes were evaluated. Behavioral performance was assessed using the Y-maze (spatial working memory), passive avoidance (associative and long-term memory), and Barnes maze tests (spatial learning and reference memory). Oxidative stress was measured via reactive oxygen species (ROS) levels. Western blot assessed autophagy-related proteins in the PI3K/AKT/mTOR (a negative regulator of autophagy) pathway. Immunofluorescence examined Iba1 (microglial activation), LC3-II (autophagy), CD86 (pro-inflammatory microglia), and NLRP3 inflammasome (a key mediator of inflammatory cell death) components. Hippocampal pro-inflammatory cytokines were quantified by ELISA.
Results |
D -galactose impaired spatial and associative memory, increased ROS, disrupted PI3K/AKT/mTOR autophagy signaling, reduced LC3-II, elevated CD86, triggered microglial pyroptosis, and caused neuroinflammation. Nano-formulated β-glucan reversed these effects, improving spatial and associative memories, reducing ROS, restoring autophagy, suppressing CD86 and pyroptosis, and attenuating neuroinflammation.
Conclusions |
β-glucan-loaded nano-niosomes exert neuroprotective effects through the simultaneous modulation of autophagy dysfunction and microglial-mediated inflammation, highlighting its potential as a therapeutic agent for neurodegenerative conditions. However, translation to human clinical practice remains uncertain and should be addressed in future studies using human-relevant models and early-phase clinical trials.
Le texte complet de cet article est disponible en PDF.Abbreviations : AD, AGEs, AKT, BBB, BDNF, CAT, CD86, CNS, DAPI, Dectin-1, DLS, ELISA, FE-SEM, GSDMD, GSH-Px, HO-1, Iba1, IL-18, IL-1β, IL-6, LC3-II, MTOR, NLRP3, Nrf2, P-AKT, PI3K, P-mTOR, P-PI3K, ROS, SASP, SCFA, SDS-PAGE, SOD, TNF-α
Keywords : Aging, D-galactose, β-glucan, Autophagy, Pyroptosis, Neuroinflammation
Plan
Vol 193
Article 118834- décembre 2025 Retour au numéro
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