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DOI: 10.1055/a-2654-7657
Neuroprotective Role of Eupalitin in Streptozotocin-Induced Diabetic Rats: In Silico and In Vivo Studies

Abstract
Alzheimerʼs disease (AD) is a neurodegenerative condition with marked cognitive loss and impaired thinking abilities as well as spatial memory, working memory, and communication skills. Numerous studies have found that both type 1 and type 2 diabetes lead to neuropathological and neurobehavioral problems, which lead to notable cognitive dysfunction and deterioration in memory. The aims of this study are to find out the neuroprotective potential of eupalitin on memory in streptozotocin-induced diabetic rats and to evaluate its in silico binding affinity on acetylcholinesterase by using molecular docking studies. Eupalitin (dose 1 mg/kg/day) was used to study the behavior model and other biochemical parameters measurement in acute as well as chronic streptozotocin (STZ)-induced diabetic rats. Eupalitin treatment increased the level of acetylcholinesterase (AChE) and lipid peroxidation and decreased glutathione in STZ-infused diabetic ratʼs brain tissue, suggesting that this substance may modulate cognitive function that is altered by oxidative stress. Results were comparable to standard drugs metformin and donepezil. Docking score and molecular mechanics generalized born surface area (MMGBSA) study results of eupalitin in comparison with donepezil possess superior predicted binding affinity toward AChE. The level of Aβ (1 – 42) was considerably lower in the eupalitin-treated group than in the STZ-treated group during both the acute and chronic phases of treatment, but results were more prominent in the case of chronic-level treatment. In silico studies showed the binding affinity toward AChE. This result concluded that eupalitin antioxidant potential may be utilized as a therapy for diabetes mellitus (DM)-related cognitive impairment.
Keywords
Alzheimerʼs disease - streptozotocin-induced - eupalitin - Nyctaginaceae - acetylcholinesterase - in silicoPublication History
Received: 06 September 2024
Accepted after revision: 17 June 2025
Article published online:
23 July 2025
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