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Pinoresinol diglucoside mitigates streptozotocin-induced cognitive decline in rats by regulating neurotransmitters, apoptosis and cytokines-NF-κB/ BDNF/ CREB/ caspase-3 pathway: Molecular docking study
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DOI：10.1016/j.lmot.2026.102242.png)
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Abstract
En 中文
Diabetes mellitus (DM) is a widespread chronic disease affecting over 300 million people globally. Prolonged hyperglycemia leads to glucotoxicity, triggering neuroinflammation, neurodegeneration, and cognitive impairment. Pinoresinol diglucoside (PDG) exhibited potent neuroprotective action; however, its potential in mitigating streptozotocin (STZ)-induced cognitive impairment remains unexplored. This study aimed to evaluate PDG's neuroprotective effects in STZ-induced cognitive deficits in male Wistar rats. The rats were randomly divided into five groups: Group I, non-diabetic control (normal saline, 1 ml/kg, p.o., twice daily for 30 days); Group II, diabetic control (STZ, 60 mg/kg, i.p., single dose, followed by normal saline, 1 ml/kg, i. p., twice daily for 30 days); Group III, PDG control (PDG, 10 mg/kg, p.o., twice daily for 30 days); Group IV, diabetic rats treated with PDG (5 mg/kg, p.o., twice daily for 30 days); and Group V, diabetic rats treated with PDG (10 mg/kg, p.o., twice daily for 30 days). DM was confirmed by elevated blood glucose levels (BGL), while cognitive function was assessed using the Y-maze and Morris water maze (MWM) tests. Following behavioural experiments, oxidative stress markers [malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), catalase (CAT)], cholinergic indices [acetylcholinesterase (AChE), choline acetyltransferase (ChAT)], neuroinflammatory cytokines [nuclear factor kappa-B (NF-kappa B), IL-6, interleukin-1R, tumor necrosis factor-alpha (TNF-alpha)], neurogenesis and cell proliferation markers [cAMP response element-binding protein (CREB), brain-derived neurotrophic factor (BDNF)], apoptosis parameter (caspase-3) and neurotransmitter dysregulation [acetylcholine (ACh), dopamine (DA)] was also validated. Molecular docking was performed to evaluate PDG's interactions with key targets. Chronic PDG treatment significantly normalized BGL, body weight (BW), improved cognitive performance, and inhibited oxidative stress. It also attenuated cholinergic dysfunction, neuroinflammation, neurogenesis and cell proliferation and apoptosis while modulating neurotransmitter levels. Docking analysis revealed strong binding affinities of PDG to AChE, DA, caspase-3, CREB, BDNF, and NF kappa B, supporting its anti-cholinesterase, anti-neuroinflammatory, and anti-apoptotic properties. These findings suggest PDG as a promising therapeutic candidate for DM-associated cognitive impairment, warranting further investigation.
Keywords:
Pinoresinol diglucoside
Cognitive impairment
Anti-neuroinflammatory
Oxidative stress
Cytokines and Molecular docking
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