ArticleInflammopharmacology2026
Neuroprotective potential of Prunetin in streptozotocin-induced cognitive dysfunction: insights from computational and experimental studies.
Article in Inflammopharmacology, 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
backgroundType 2 diabetes mellitus (T2DM) accounts for over 85% of global diabetes cases and is strongly associated with cognitive decline resulting from chronic hyperglycemia-induced neuronal and oxidative damage. Prunetin, a natural isoflavone known for potent antioxidant and antidiabetic activity, was investigated for its potential to attenuate diabetes-associated cognitive deficits.
methodsIn silico analysis included molecular docking, MM-GBSA binding free energy, and molecular dynamics simulations (100 ns) to explore interactions between Prunetin and human acetylcholinesterase (AChE; PDB ID: 7D9O). In vivo studies were conducted in streptozotocin (STZ)-induced diabetic rats, with cognition assessed using the Morris water maze. Brain tissues were examined for Aβ(1-42), lipid peroxidation, reduced glutathione (GSH), and AChE activity to determine oxidative status and cholinergic function.
resultsPrunetin (0.5 mg/kg/day) administered for 14 (acute) or 28 days (chronic) reduced blood glucose levels, Aβ(1-42) accumulation, and lipid peroxidation while increasing GSH levels and inhibiting AChE activity in a duration-dependent manner. These effects corresponded with significant improvements in Morris water maze performance, with 28-day treatment demonstrating greater efficacy than the 14-day regimen for most parameters. Computational modeling confirmed stable Prunetin-AChE complex formation mediated by hydrogen bonding, hydrophobic interactions, and π-π stacking interactions.
conclusionPrunetin demonstrates notable antioxidant and AChE-inhibitory properties, attenuating STZ-induced cognitive dysfunction in an experimental rat model. These findings collectively support Prunetin as a promising multitarget candidate warranting further investigation for diabetes-associated neurodegeneration.
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