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. Author manuscript; available in PMC: 2011 Jan 1.
Published in final edited form as: Stroke. 2009 Nov 12;41(1):166–172. doi: 10.1161/STROKEAHA.109.561852

Fig. 3. TAT-AIP treatment confers neuroprotection against H-I in P7 rats.

Fig. 3

(A) Western blotting with the anti-HA antibody shows that intraperitoneal injection of TAT-AIP (12 mg/kg, 0 and 6 hr after H-I) results in transduction of the protein (molecular size: ~21 kDa) into the cerebral cortex and hippocampus. Injection of AIP without TAT serves as a negative control. The graph (lower panel) summarizes the results from 4 sets of samples. (B) Double-label immunofluorescent staining of TAT-AIP (anti-HA) and NeuN in the cortex at 3 hr after protein injection. Immunoreactivity is detected in a large number of neurons (d-f) after TAT-AIP injection; the signals are abolished in sections (g-i) pre-absorbed with the recombinant TAT-AIP (10 μg/ml). Immunoreactivity is also not detected in brain receiving AIP injection (a-c). (C) H-E staining 7 days after H-I show improved histology in TAT-AIP-treated rat brains. Panels a-c, the arrows point to the injured hemisphere; panels d-f, low-power images of the dorsal hippocampus; panels g-j, high-power images (magnification ×200) of cortex after sham surgery (g) or after H-I (h-j); panels k-n, high-power images of striatum after sham surgery (k) or after H-I (l-n). (B) Brain tissue loss was measured 7 days after H-I. *p<0.05; **p<0.01 vs. vehicle treatment (n=12–15/group).