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. Author manuscript; available in PMC: 2006 Jul 24.
Published in final edited form as: Neurosurgery. 2005 Mar;56(3):590–604. doi: 10.1227/01.NEU.0000154060.14900.8F

FIGURE 3.

FIGURE 3

DFU treatment attenuated COX2 expression after TBI. DFU (10 mg/kg initiated 10 min before injury, right columns) reduced COX2 in both ipsilateral parietal cortex (A) and hippocampal CA2–CA3 regions (B) compared with vehicle-treated controls (left columns). Attenuation of COX2-ir was observed as early as 6 hours (top panels), at 24 hours (middle), and at 72 hours (bottom) after injury. COX2-ir was evaluated in 3 to 4 animals per group, according to both the cell number and the intensity of signal (see Materials and Methods). Scale bar = 50 μm. C, immunoblots of COX2 (72 kD) from the ipsilateral cortex (left) and hippocampus (right) at 72 hours after injury. DFU attenuated injury-induced COX2 in the ipsilateral cortex (P < 0.05, Dunnett’s test) but not in the hippocampus (right) by this method. Fresh-frozen micropunches of injured cortex and dorsal hippocampus (bregma − 3.6 to − 4.3 mm according to the coordinates of Paxinos and Watson [74]) were dissected and processed as described (96).

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