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Oleanolic acid protects against optic nerve degeneration and retinal ganglion cells loss in an experimental model of multiple sclerosis

AuthorsCordova, Claudia; Gutiérrez, Beatriz; Martín, Rubén ; Hernández, Marita ; Téllez, Nieves; Nieto, María Luisa
Issue Date2015
CitationECTRIMS (2015)
AbstractMultiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS) that currently lacks neuroprotective treatments. In many patients optic neuritis (ON) is the first clinically symptom. Experimental autoimmune encephalomyelitis (EAE), an animal model of MS, affects spinal cord, brain and optic nerves causing ON, among others disabilities. ON occurs as a result of inflammation, oxidative stress, demyelination, axonal damage in the optic nerve followed by retinal ganglion cell (RGC) loss. Our goal was to determine the usefulness of the triterpene, oleanolic acid (OA) in preventing ON with a focus on neuroprotection. [Methods]: OA (50 mg/kg/day) was i.p. administered to MOG35-55 immunized-C57/BL6 mice from immunization to day 45. Eyeballs were cut through the pupillary-optic nerve plane and optic nerve was cut longitudinally. Sections were stained with hematoxylin and eosin (inflammation), luxol fast blue (demyelination), toluidine blue (RGC counts), tunel (apoptosis) and Fluoro-Jade® B (axonal degeneration). RGC were counted on 3 standard areas. Glutamate concentration was determined with a Glutamate Assay Kit. [Results]: Histopathological analysis of optic nerves showed presence of cell infiltration, myelin loss as well as swollen and distorted axons in untreated-EAE mice, whereas these effects were not detectable in sections from healthy or OA-treated EAE mice. We found that the number of apoptotic cells and degenerated axons (Fluoro-Jade® B+) were lower in optic nerve sections from OA treated-EAE mice than in the untreated-EAE group. Apoptotic cells in untreated-EAE mice were enhanced over 3-4 fold compared to healthy mice (p< 0.001), while in samples from OA-treated EAE mice the apoptotic cells only increased 1.6 fold (p< 0.001). At the same time, glutamate levels in optic nerve decreased from 16.6 ± 2.8 mM, in untreated EAE mice, to 3.5 ± 0.2 mM in OA-treated EAE mice (p< 0.001), with the concentration in controls being 0.7 ± 0.3 mM. In addition, EAE caused a significant loss of cells by an average of 39.35% (p< 0.001) in the RGC layer, which was eliminated in OA-treated EAE mice. [Conclusion]: OA suppresses inflammation, reduces demyelination, axonal injury, and promotes RGC survival during experimental optic neuritis. This study provides new findings regarding the neuroprotective activity of OA in EAE.
DescriptionResumen del póster presentado al 31st Congress of the European Committee for Treatment and Research in Multiple Sclerosis, celebrado en barcelona (España) del 7 al 10 de octubre de 2015.-- et al.
Appears in Collections:(IBGM) Comunicaciones congresos
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