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; Emadyan, Omid

doi:10.1016/j.neulet.2006.08.033

Cited by 30 publications

(19 citation statements)

References 25 publications

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“…4). This is in line with previous published data showing increase in CD4 + T cells [27], [30], demyelination [32], and lesion size [28] with increasing EAE severity. Overall we observed a parallel increase in demyelination, F480 + macrophage and CD3 + T cell infiltration in the CNS with an increase in EAE severity.…”

Section: Resultssupporting

confidence: 93%

Global and 3D Spatial Assessment of Neuroinflammation in Rodent Models of Multiple Sclerosis

et al. 2013

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Multiple Sclerosis (MS) is a progressive autoimmune inflammatory and demyelinating disease of the central nervous system (CNS). T cells play a key role in the progression of neuroinflammation in MS and also in the experimental autoimmune encephalomyelitis (EAE) animal models for the disease. A technology for quantitative and 3 dimensional (3D) spatial assessment of inflammation in this and other CNS inflammatory conditions is much needed. Here we present a procedure for 3D spatial assessment and global quantification of the development of neuroinflammation based on Optical Projection Tomography (OPT). Applying this approach to the analysis of rodent models of MS, we provide global quantitative data of the major inflammatory component as a function of the clinical course. Our data demonstrates a strong correlation between the development and progression of neuroinflammation and clinical disease in several mouse and a rat model of MS refining the information regarding the spatial dynamics of the inflammatory component in EAE. This method provides a powerful tool to investigate the effect of environmental and genetic forces and for assessing the therapeutic effects of drug therapy in animal models of MS and other neuroinflammatory/neurodegenerative disorders.

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Section: Resultssupporting

confidence: 93%

Global and 3D Spatial Assessment of Neuroinflammation in Rodent Models of Multiple Sclerosis

et al. 2013

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“…As ROS was elevated in the progression of EAE, anti-oxidants such as SOD and GSH-Px were found synchronously to be gradually decreased, especially at early stages of the disease [39]. SOD catalyzes the dismutation of superoxide anion to hydrogen peroxide.…”

Section: Discussionmentioning

confidence: 99%

Astragaloside IV Attenuates Experimental Autoimmune Encephalomyelitis of Mice by Counteracting Oxidative Stress at Multiple Levels

Gao

et al. 2013

PLoS ONE

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Multiple sclerosis (MS) is a chronic autoimmune neuroinflammatory disease found mostly in young adults in the western world. Oxidative stress induced neuronal apoptosis plays an important role in the pathogenesis of MS. In current study, astragaloside IV (ASI), a natural saponin molecule isolated from Astragalus membranceus, given at 20 mg/kg daily attenuated the severity of experimental autoimmune encephalomyelitis (EAE) in mice significantly. Further studies disclosed that ASI treatment inhibited the increase of ROS and pro-inflammatory cytokine levels, down-regulation of SOD and GSH-Px activities, and elevation of iNOS, p53 and phosphorylated tau in central nervous system (CNS) as well as the leakage of BBB of EAE mice. Meanwhile, the decreased ratio of Bcl-2/Bax was reversed by ASI. Moreover, ASI regulated T-cell differentiation and infiltration into CNS. In neuroblast SH-SY5Y cells, ASI dose-dependently reduced cellular ROS level and phosphorylation of tau in response to hydrogen peroxide challenge by modulation of Bcl-2/Bax ratio. ASI also inhibited activation of microglia both in vivo and in vitro. iNOS up-regulation induced by IFNγ stimulation was abolished by ASI dose-dependently in BV-2 cells. In summary, ASI prevented the severity of EAE progression possibly by counterbalancing oxidative stress and its effects via reduction of cellular ROS level, enhancement of antioxidant defense system, increase of anti-apoptotic and anti-inflammatory pathways, as well as modulation of T-cell differentiation and infiltration into CNS. The study suggested ASI may be effective for clinical therapy/prevention of MS.

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“…Interestingly, low GSH levels are associated with many autoimmune, and inflammatory diseases, including Rheumatoid Arthritis (Hassan et al, 2001), systemic lupus erythematous (Perl et al, 2004), Crohn’s disease (Sido et al, 1998), multiple sclerosis (Zargari et al, 2007), psoriasis (Kokcam and Naziroglu, 1999), and contact dermatitis (Eisen et al, 2004). However, because this list of diseases does not fall exclusively into the category of a Th1-dominant or Th2-dominant disorder, it suggests that compromised GSH levels may be a more critical factor in the initial onset of these conditions.…”

Section: Inflammatory and Immune System Diseasesmentioning

confidence: 99%

Glutathione dysregulation and the etiology and progression of human diseases

Ballatori

Krance

Notenboom

et al. 2009

BCHM

901

656

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Glutathione (GSH) plays an important role in a multitude of cellular processes, including cell differentiation, proliferation, and apoptosis, and as a result, disturbances in GSH homeostasis are implicated in the etiology and/or progression of a number of human diseases, including cancer, diseases of aging, cystic fibrosis, and cardiovascular, inflammatory, immune, metabolic, and neurodegenerative diseases. Owing to the pleiotropic effects of GSH on cell functions, it has been quite difficult to define the role of GSH in the onset and/or the expression of human diseases, although significant progress is being made. GSH levels, turnover rates, and/or oxidation state can be compromised by inherited or acquired defects in the enzymes, transporters, signaling molecules, or transcription factors that are involved in its homeostasis, or from exposure to reactive chemicals or metabolic intermediates. GSH deficiency or a decrease in the GSH/glutathione disulfide ratio manifests itself largely through an increased susceptibility to oxidative stress, and the resulting damage is thought to be involved in diseases, such as cancer, Parkinson's disease, and Alzheimer's disease. In addition, imbalances in GSH levels affect immune system function, and are thought to play a role in the aging process. Just as low intracellular GSH levels decrease cellular antioxidant capacity, elevated GSH levels generally increase antioxidant capacity and resistance to oxidative stress, and this is observed in many cancer cells. The higher GSH levels in some tumor cells are also typically associated with higher levels of GSH-related enzymes and transporters. Although neither the mechanism nor the implications of these changes are well defined, the high GSH content makes cancer cells chemoresistant, which is a major factor that limits drug treatment. The present report highlights and integrates the growing connections between imbalances in GSH homeostasis and a multitude of human diseases.

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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

Cited by 30 publications

References 25 publications

Global and 3D Spatial Assessment of Neuroinflammation in Rodent Models of Multiple Sclerosis

Global and 3D Spatial Assessment of Neuroinflammation in Rodent Models of Multiple Sclerosis

Astragaloside IV Attenuates Experimental Autoimmune Encephalomyelitis of Mice by Counteracting Oxidative Stress at Multiple Levels

Glutathione dysregulation and the etiology and progression of human diseases

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