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

Figure 13

C16 treatment reduced TNF-α expression both in spinal cord and brain. TNF-α immunostaining, counterstained with hematoxylin; bar = 100 μm. ((a), (c), (e), (g), (i), (k), and (m) Coronal sections of motor cortex; (b), (d), (f), (h), (j), (l), and (n) traverse section through the lumbar spinal cord). At 2 weeks after immunization: vehicle control rats ((a), (b) plenty of TNF-α labeled apoptotic neural cells appeared in motor cortex and spinal cord anterior horn), 2 mg/per day C16 treated EAE rats ((c), (d)), and C16 late treated EAE rats ((e), (f)). At week 8 after immunization, vehicle control rats ((g), (h)), 2 mg/per day C16 treated EAE rats ((i), (j)), and C16 late treated EAE rats ((k), (l)). (k) Medium to high-dose C16 treatment reduced TNF-α labeled cells at 2 weeks postimmunization group, ^a𝑃<0.05 versus normal rats; ^b𝑃<0.05 versus vehicle control rats, ^c𝑃<0.05 versus 0.5 mg/per day C16 treated EAE rats. At week 8 after immunization, ^f𝑃<0.05 versus vehicle control rats, ^g𝑃<0.05 versus 0.5 mg/per day C16 treated EAE rats, and ^h𝑃<0.05 versus 1 mg/per day C16 treated EAE rats. (l) Late treated C16 treatment also decreased TNF-α labeled cells to a certain extent. ^a𝑃<0.05 versus normal rats; ^b𝑃<0.05 versus vehicle control rats at week 2 after immunization; ^c𝑃<0.05 versus C16 treated EAE rats at week 2 after immunization; ^d𝑃<0.05 versus vehicle control rats at week 8 after immunization.

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