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

Figure 9

The C16 treatment inhibited reactive gliosis revealed by FITC-conjugated GFAP immunofluorescent staining; traverse section through the lumbar spinal cord; bar = 100 μm. At week 8 after immunization, normal rats group (a), vehicle control rats (b), 0.5 mg (c), 1 mg/per day C16 treated EAE rats (d), and 2 mg/per day C16 treated EAE rats (e). Vehicle late treated EAE rats (f) and C16 late treated EAE rats (g) at week 2 after immunization. Vehicle late treated EAE rats (h) and C16 late treated EAE rats (i) at week 8 post-immunization. Medium and high dose C16 treatment reduced reactive gliosis (j). ^a𝑃<0.05 versus normal rats, ^b𝑃<0.05 versus vehicle control rats, and ^c𝑃<0.05 versus 0.5 mg/per day C16 treated EAE rats at week 8 after immunization. (k) Late treated C16 treatment also inhibited reactive gliosis to a certain extent. ^a𝑃<0.05 versus normal rats; ^b𝑃<0.05 versus vehicle control rats; ^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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