Cited by 20Neurological Disease Mechanisms and TreatmentsCircadian rhythm and melatoninNeurological Disorders and Treatments

Melatonin Ameliorates Brain Oxidative Stress and Upregulates Senescence Marker Protein-30 and Osteopontin in a Rat Model of Vascular Dementia

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Bin-Jaliah, I, Sakr, HF·2018·Physiology International

Abstract

The aim of this study was to investigate the effect of melatonin on oxidative stress and senescence marker protein-30 (SMP30) as well as osteopontin (OPN) expression in the hippocampus of rats subjected to vascular dementia (VD). A total of 72 male rats were divided into six groups (n = 12 each) as follows: (i) untreated control (CON), (ii) sham-operated group, (iii) sham-operated + melatonin, (iv) rats exposed to VD induced by permanent bilateral occlusion of the common carotid arteries (BCCAO) leading to chronic cerebral hypoperfusion, (v) rats exposed to VD + melatonin, and (vi) rats exposed to VD + donepezil (DON). At the end of experiment, the hippocampal levels of acetylcholine (ACh), norepinephrine (NE), and dopamine (Dop) were measured. Expression of OPN was determined using immunohistochemistry, and SMP30 expression was determined using real-time PCR in the hippocampus. Hippocampal thiobarbituric acid reactive substances (TBARS) and total antioxidant capacity (TAC) were evaluated. The BCCAO group showed significantly decreased TAC (p < 0.05) and significantly increased in TBARS levels compared with the CON group. In addition, BCCAO significantly decreased (p < 0.05) the expression of both OPN and SMP30 and the levels of ACh, NE, and Dop in the hippocampus compared with CON treatment. Treatment with melatonin significantly increased OPN and SMP30 expression and ACh, NE, and Dop levels in the hippocampus with amelioration of the oxidative stress compared with BCCAO rats. Melatonin might produce a neuroprotective effect through its antioxidant action and by increasing the expression of SMP30 and OPN that is not comparable with that of DON.

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Crossref · 10.1556/2060.105.2018.1.1

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  • In vascular demented rats, melatonin treatment ameliorates brain oxidative stress and increases osteopontin and senescence marker protein-30.

    “Finally, brain oxidative stress amelioration and increased osteopontin and senescence marker protein-30 have been shown following melatonin treatment in the context of vascular demented rats [466].”

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Authors
Bin-Jaliah, I., & Sakr, H.
Affiliations
  • 1 Department of Physiology, College of Medicine, King Khalid University, Abha, Saudi Arabia
  • Mansoura University (EG)
Venue
Physiology International
Published
2018-03
Volume
105
Issue
1
Pages
38-52
ISSN
2498-602X (ISSN-L)
OpenAlex
W2795228647
Cited by
20
References
56
Citations by year
2025: 1 · 2024: 2 · 2022: 6 · 2021: 6 · 2020: 3 · 2019: 1 · 2018: 1
FWCI
1.23
Type
journal article
Language
en
Open access
Locations
  • Physiology International (publishedVersion)
  • PubMed (publishedVersion)
  • Repository of the Academy's Library (Library of the Hungarian Academy of Sciences) (acceptedVersion)
Funders
  • King Khalid University
  • Mansoura University
Topics
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
Keywords
melatonin, vascular dementia, oxidative stress, SMP30, osteopontin, hippocampus, chronic cerebral hypoperfusion, bilateral common carotid artery occlusion, donepezil, acetylcholine, norepinephrine, dopamine, neuroprotection, antioxidant capacity, lipid peroxidation
MeSH terms
Acetylcholine, Animals, Antioxidants, Calcium-Binding Proteins, Carboxylic Ester Hydrolases, Disease Models, Animal, Dopamine, Hippocampus, Male, Melatonin, Norepinephrine, Dementia, Vascular, Up-Regulation, Rats, Sprague-Dawley, Apoptosis, Oxidative Stress, Proto-Oncogene Proteins c-bcl-2, Intracellular Signaling Peptides and Proteins, bcl-2-Associated X Protein, Osteopontin

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