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. Author manuscript; available in PMC: 2013 Jan 7.
Published in final edited form as: J Cereb Blood Flow Metab. 2008 Dec 3;29(3):524–533. doi: 10.1038/jcbfm.2008.142

Figure 1.

Figure 1

Immunohistochemistry and histopathology 4 h after FPI. Sections of the parietal cortex from piglet brains after FPI (A–C, F, L, newborn vehicle; D, E, newborn-EEIIMD 1 mg/kg i.v.; G–I, juvenile-vehicle; J, K, juvenile-EEIIMD) and from uninjured control animal (M–O, newborn vehicle), were subjected to antigen retrieval in citrate buffer and stained with anti-phospho-ERK rabbit monoclonal antibody (2 μg/mL) (no. 4376; Cell Signaling) (A, D, G, J, M), or with anti-uPA monoclonal antibody (5 μg/mL) (no. 3689; American Diagnostica) (B, E, H, K, N), with mouse anti-neuronal nuclei monoclonal antibody (5 μg/mL) as a neuronal marker (no. MAB377; Chemicon International, Billerica, MA, USA) (C), or with nonimmune mouse IgG1 as a negative control (F), secondary biotinylated anti-mouse IgG (1:200), followed by incubation with HRP-conjugated streptavidin. Magnification shown is ×400 for all panels except (I, L) which was ×100 and ×1,000 for inserts in (A, C). Adjacent sections from the same brains exposed to brain injury (I, L) and from uninjured control (O), were stained by H&E for histologic inspection. These data reflect an n of 2 per experimental group.