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Relationship between the clinical scoring and demyelination in central nervous system with total antioxidant capacity of plasma during experimental autoimmune encephalomyelitis development in mice

Zargari, Mehryar ; Allameh, Abdolamir ; Sanati, Mohammad Hossein ; Tiraihi, Taki ; Lavasani, Shahram LU and Emadyan, Omid (2007) In Neuroscience Letters 412(1). p.24-28
Abstract
Experimental autoimmune encephalomyelitis (EAE) was induced in a mouse model (C57/BL6) to investigate the antioxidant status of animals at various clinical stages of the disease. For this purpose, blood, brain and spinal cord samples from EAE mice were collected and examined at different scores following post-immunization with myelin oligodendrocyte glycoprotein (MOG). The clinical sign of mobility of animals on different days was associated with gradual increase in lipid peroxidation products (malondialdehyde, i.e. NIDA) in brain and spinal cord. Changes in lipid peroxidation during EAE progression was inversely related to superoxide dismutase (SOD) activity in erythrocyte preparation. However, suppression of catalase in erythrocytes,... (More)
Experimental autoimmune encephalomyelitis (EAE) was induced in a mouse model (C57/BL6) to investigate the antioxidant status of animals at various clinical stages of the disease. For this purpose, blood, brain and spinal cord samples from EAE mice were collected and examined at different scores following post-immunization with myelin oligodendrocyte glycoprotein (MOG). The clinical sign of mobility of animals on different days was associated with gradual increase in lipid peroxidation products (malondialdehyde, i.e. NIDA) in brain and spinal cord. Changes in lipid peroxidation during EAE progression was inversely related to superoxide dismutase (SOD) activity in erythrocyte preparation. However, suppression of catalase in erythrocytes, tissue glutathione (GSH) and plasma total antioxidant capacity (FRAP assay) were the early events in EAE, occurred during scores 1 and 2. Biochemical alterations were corroborated with histopathological observations showing demyelination and inflammatory foci in central nervous system (CNS) of animals suffering from partial hind limb paralysis (score 3). These data suggest that generation of NIDA in CNS is a continuous process during EAE induction and suppression of antioxidant factors are early events of the disease, but crucial in increasing the vulnerability of CNS to demyelinating lesions. (Less)
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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
experimental autoimmune encephalomyelitis (EAE), antioxidant, demyelination
in
Neuroscience Letters
volume
412
issue
1
pages
24 - 28
publisher
Elsevier
external identifiers
  • wos:000244140400005
  • scopus:33845947272
ISSN
0304-3940
DOI
10.1016/j.neulet.2006.08.033
language
English
LU publication?
yes
id
a38a9c47-af21-4898-809f-a0e36c0f24a9 (old id 674493)
date added to LUP
2016-04-01 11:57:33
date last changed
2022-01-26 20:43:59
@article{a38a9c47-af21-4898-809f-a0e36c0f24a9,
  abstract     = {{Experimental autoimmune encephalomyelitis (EAE) was induced in a mouse model (C57/BL6) to investigate the antioxidant status of animals at various clinical stages of the disease. For this purpose, blood, brain and spinal cord samples from EAE mice were collected and examined at different scores following post-immunization with myelin oligodendrocyte glycoprotein (MOG). The clinical sign of mobility of animals on different days was associated with gradual increase in lipid peroxidation products (malondialdehyde, i.e. NIDA) in brain and spinal cord. Changes in lipid peroxidation during EAE progression was inversely related to superoxide dismutase (SOD) activity in erythrocyte preparation. However, suppression of catalase in erythrocytes, tissue glutathione (GSH) and plasma total antioxidant capacity (FRAP assay) were the early events in EAE, occurred during scores 1 and 2. Biochemical alterations were corroborated with histopathological observations showing demyelination and inflammatory foci in central nervous system (CNS) of animals suffering from partial hind limb paralysis (score 3). These data suggest that generation of NIDA in CNS is a continuous process during EAE induction and suppression of antioxidant factors are early events of the disease, but crucial in increasing the vulnerability of CNS to demyelinating lesions.}},
  author       = {{Zargari, Mehryar and Allameh, Abdolamir and Sanati, Mohammad Hossein and Tiraihi, Taki and Lavasani, Shahram and Emadyan, Omid}},
  issn         = {{0304-3940}},
  keywords     = {{experimental autoimmune encephalomyelitis (EAE); antioxidant; demyelination}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{24--28}},
  publisher    = {{Elsevier}},
  series       = {{Neuroscience Letters}},
  title        = {{Relationship between the clinical scoring and demyelination in central nervous system with total antioxidant capacity of plasma during experimental autoimmune encephalomyelitis development in mice}},
  url          = {{http://dx.doi.org/10.1016/j.neulet.2006.08.033}},
  doi          = {{10.1016/j.neulet.2006.08.033}},
  volume       = {{412}},
  year         = {{2007}},
}