Dose-Dependent Anti-Inflammatory and Neuroprotective Effects of an ανβ3 Integrin-Binding Peptide

Figure 5

C16 treatment alleviated axonal loss in spinal cord and cerebral cortex revealed by Bielschowsky staining both at weeks 2 and 8 after immunization. ((a), (c), (g), (i), and (k) coronal sections of motor cortex; (b), (d), (e), (f), (h), and (j) traverse sections through the lumbar spinal cord); bar = 100 μm. At week 2 after immunization, normal rats group ((a), (b)), vehicle control rats ((c) axons were undergoing gradual loss and exhibiting deformed and ovoid formation; (d) an arrow shows the axon loss in white matter); 2 mg/per day C16 treated EAE rats (e) and C16 late treated EAE rats (f). At week 8 after immunization, vehicle control rats ((g), (h)), 2 mg/per day C16 treated EAE rats ((i), (j)). C16 late treated EAE rats ((k), (l)). (m) Medium to high-dose C16 treatment prevented axon loss by an estimate of axonal loss score. ^a𝑃<0.05 versus normal rats; ^b𝑃<0.05 versus vehicle control rats at week 2 after immunization group; ^f𝑃<0.05 versus vehicle control rats at week 8 after immunization. ^g𝑃<0.05 versus 0.5 mg/per day C16 treated EAE rats at week 8 after immunization. (n) C16 late treatment prevented demyelination to a certain extent by axonal loss score. ^a𝑃<0.05 versus normal rats; ^b𝑃<0.05 versus vehicle control rats at week 2 postimmunization group; ^c𝑃<0.05 versus C16 treated EAE rats at week 2 postimmunization group; ^d𝑃<0.05 versus vehicle control rats at week 8 after immunization.

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