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Arbutin Intervention Ameliorates Memory Impairment in a Rat Model of Lysolecethin Induced Demyelination: Neuroprotective and Anti-Inflammatory Effects Publisher Pubmed



Ashrafpour S1, 2 ; Nasrtaherabadi MJ2 ; Sabourirad A2 ; Hosseinzadeh S3 ; Pourabdolhossein F4, 5
Authors
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Authors Affiliations
  1. 1. Mobility Impairment Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
  2. 2. Student Research Committee, Babol University of Medical Sciences, Babol, Iran
  3. 3. Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran
  5. 5. Department of Physiology, School of Medicine, Babol University of Medical Sciences, Babol, Iran

Source: Behavioural Brain Research Published:2024


Abstract

Cognitive impairment (CI) and memory deficit are prevalent manifestations of multiple sclerosis (MS). This study explores the therapeutic potential of arbutin on memory deficits using a rat hippocampal demyelination model induced by lysophosphatidylcholine (LPC). Demyelination was induced by bilateral injection of 1% LPC into the CA1 area of the hippocampus, and the treated group received daily arbutin injections (50 mg/kg, i.p) for two weeks. Arbutin significantly improved memory impairment 14 days post-demyelination as assessed by Morris water maze test. Histological and immunohistochemical analyses demonstrated that arbutin reduced demyelination suppressed pro-inflammatory markers (IL-1β, TNF-α) and increased anti-inflammatory cytokine IL-10. Arbutin also diminished astrocyte activation, decreased iNOS, enhanced anti-oxidative factors (Nrf2, HO-1), and exhibited neuroprotective effects by elevating myelin markers (MBP) and brain derived neurotrophic factor (BDNF). These findings propose arbutin as a potential therapeutic candidate for multiple sclerosis-associated memory deficits, warranting further clinical exploration. © 2024 Elsevier B.V.
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