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Axonal damage and oxidative stress during chronic experimental allergic encephalomyelitis

Axonal damage and oxidative stress during chronic experimental allergic encephalomyelitis
Axonal damage and oxidative stress during chronic experimental allergic encephalomyelitis
Objectives
In the chronic disabling disease multiple sclerosis (MS), migration of monocytes across the blood-brain barrier is a crucial step in the formation of lesions in the central nervous system (CNS). Here we investigate whether infiltrating monocyte-derived macrophages contribute to axonal demyelination and damage by the secretion of oxygen radicals in chronic experimental allergic encephalomyelitis (EAE), the animal model for MS
Methodology
Chronic EAE was induced in Dark Agouti rats and animals were sacrificed at various time points. Axonal damage and oxygen radicals were detected by immunohistochemistry for the accumulation of amyloid precursor protein (APP) and dephosphorylated neurofilament and nitrotyrosine, respectively. Chronic EAE animals were treated with luteolin, a naturally occurring dietary anti-oxidant, to study the involvement of oxygen radicals in the course of the disease.
Results
Axonal damage, as demonstrated by amyloid precursor protein accumulation and dephosphorylation of neurofilaments, is evident in both early and late stages of chronic EAE. Axonal damage was abundant in macrophage-infiltrated areas of the CNS of diseased animals. Luteolin treatment reduced cellular infiltration, oxidative stress as detected by nitrotyrosine levels and axonal damage in the CNS of EAE animals.
Conclusion T hese data suggest that macrophages contribute to axonal damage in EAE and that anti-oxidants may have a protective role in CNS inflammation and axonal damage as observed in MS and EAE.
macrophages, axonal damage, multiple sclerosis, oxidative stress, flavonoids
171-176
Hendriks, J.J.A
63334f84-cab1-491b-823e-55394504938b
van Meeteren, M.E.
79c9b4ba-6519-4d17-964b-78ac3f98d19d
van der Pol, S.M.A.
04465ccd-84b6-477a-88e4-b6fb08a6692c
Newman, T.A.
322290cb-2e9c-445d-a047-00b1bea39a25
Dijkstra, C.D.
37e7c411-db4c-4ea6-b290-ca1317651840
de Vries, H.E.
1ea05eab-3f4f-4156-a244-05988c06cf22
Hendriks, J.J.A
63334f84-cab1-491b-823e-55394504938b
van Meeteren, M.E.
79c9b4ba-6519-4d17-964b-78ac3f98d19d
van der Pol, S.M.A.
04465ccd-84b6-477a-88e4-b6fb08a6692c
Newman, T.A.
322290cb-2e9c-445d-a047-00b1bea39a25
Dijkstra, C.D.
37e7c411-db4c-4ea6-b290-ca1317651840
de Vries, H.E.
1ea05eab-3f4f-4156-a244-05988c06cf22

Hendriks, J.J.A, van Meeteren, M.E., van der Pol, S.M.A., Newman, T.A., Dijkstra, C.D. and de Vries, H.E. (2005) Axonal damage and oxidative stress during chronic experimental allergic encephalomyelitis. Journal of Neuroprotection and Neuroregeneration, 1 (3), 171-176.

Record type: Article

Abstract

Objectives
In the chronic disabling disease multiple sclerosis (MS), migration of monocytes across the blood-brain barrier is a crucial step in the formation of lesions in the central nervous system (CNS). Here we investigate whether infiltrating monocyte-derived macrophages contribute to axonal demyelination and damage by the secretion of oxygen radicals in chronic experimental allergic encephalomyelitis (EAE), the animal model for MS
Methodology
Chronic EAE was induced in Dark Agouti rats and animals were sacrificed at various time points. Axonal damage and oxygen radicals were detected by immunohistochemistry for the accumulation of amyloid precursor protein (APP) and dephosphorylated neurofilament and nitrotyrosine, respectively. Chronic EAE animals were treated with luteolin, a naturally occurring dietary anti-oxidant, to study the involvement of oxygen radicals in the course of the disease.
Results
Axonal damage, as demonstrated by amyloid precursor protein accumulation and dephosphorylation of neurofilaments, is evident in both early and late stages of chronic EAE. Axonal damage was abundant in macrophage-infiltrated areas of the CNS of diseased animals. Luteolin treatment reduced cellular infiltration, oxidative stress as detected by nitrotyrosine levels and axonal damage in the CNS of EAE animals.
Conclusion T hese data suggest that macrophages contribute to axonal damage in EAE and that anti-oxidants may have a protective role in CNS inflammation and axonal damage as observed in MS and EAE.

Full text not available from this repository.

More information

Submitted date: 3 March 2005
Published date: July 2005
Keywords: macrophages, axonal damage, multiple sclerosis, oxidative stress, flavonoids

Identifiers

Local EPrints ID: 58250
URI: https://eprints.soton.ac.uk/id/eprint/58250
PURE UUID: 4faf69ee-9480-4467-8b59-b63495715f08
ORCID for T.A. Newman: ORCID iD orcid.org/0000-0002-3727-9258

Catalogue record

Date deposited: 12 Aug 2008
Last modified: 14 Mar 2019 01:51

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