Acute Experimental Allergic Encephalomyelitis Increases Lumbar Spinal Cord Incorporation of Epidurally Administered [3H]-D-Mannitol and [14C]-Carboxyl-Inulin in Rabbits

Naidu, K. Akhilender; Fu, Eugene S.; Prockop, Leon D.

doi:10.1097/00000539-200201000-00040

Cited by 2 publications

(1 citation statement)

References 17 publications

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“…The rats in the normal control group were injected with CFA emulsified 1 : 1 with 0.9% saline [5, 20]. Immediately after CFA injection, and again after 48 hours, the rats received intraperitoneal injection of 300 ng Pertussis toxin (Sigma) twice.…”

Section: Methodsmentioning

confidence: 99%

Dose-Dependent Anti-Inflammatory and Neuroprotective Effects of anανβ3 Integrin-Binding Peptide

Han

Zhang

et al. 2013

Mediators of Inflammation

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Previous studies have shown that prevention of leukocyte infiltration by targeting integrins involved in transendothelial migration may suppress the clinical and pathological features of neuroinflammatory disease. This study was designed to investigate the effects of C16, an α ν β3 integrin-binding peptide, in an acute experimental allergic encephalomyelitis (EAE) rat model. Multiple histological and immunohistochemical staining, electron microscopy observation, ELISA assay, Western blot, and magnetic resonance imaging (MRI) were employed to assess the degree of inflammation, axonal loss, neuronal apoptosis, white matter demyelination, and extent of gliosis in the brain and spinal cord of differently treated EAE models. The results showed that C16 treatment could inhibit extensive leukocyte and macrophage accumulation and infiltration and reduce cytokine tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) expression levels. A significantly lower clinical score at the peak time of disease was also demonstrated in the C16 treated group. Moreover, astrogliosis, demyelination, neuronal death, and axonal loss were all alleviated in C16 treated EAE animals, which may be attributed to the improvement of microenvironment. The data suggests that C16 peptide may act as a protective agent by attenuating inflammatory progression and thus affecting the expression of some proinflammatory cytokines during neuroinflammatory disease.

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Section: Methodsmentioning

confidence: 99%

Dose-Dependent Anti-Inflammatory and Neuroprotective Effects of anανβ3 Integrin-Binding Peptide

Han

Zhang

et al. 2013

Mediators of Inflammation

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Animal Models of Multiple Sclerosis

Young

Welsh

2008

Sourcebook of Models for Biomedical Research

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To determine whether an immunological or pharmaceutical product has potential for therapy in treating multiple sclerosis (MS), detailed animal models are required. To date many animal models for human MS have been described in mice, rats, rabbits, guinea pigs, marmosets, and rhesus monkeys. The most comprehensive studies have involved murine experimental allergic (or autoimmune) encephalomyelitis (EAE), Semliki Forest virus (SFV), mouse hepatitis virus (MHV), and Theiler's murine encephalomyelitis virus (TMEV). Here, we describe in detail multispecies animal models of human MS, namely EAE, SFV, MHV, and TMEV, in addition to chemically induced demyelination. The validity and applicability of each of these models are critically evaluated.

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Acute Experimental Allergic Encephalomyelitis Increases Lumbar Spinal Cord Incorporation of Epidurally Administered [3H]-D-Mannitol and [14C]-Carboxyl-Inulin in Rabbits

Cited by 2 publications

References 17 publications

Dose-Dependent Anti-Inflammatory and Neuroprotective Effects of anανβ3 Integrin-Binding Peptide

Dose-Dependent Anti-Inflammatory and Neuroprotective Effects of anανβ3 Integrin-Binding Peptide

Animal Models of Multiple Sclerosis

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