Fig. 6.

Cleavage of procaspase 3 to active fragments occurs at 24 hr after neonatal hypoxia–ischemia. A, Top, Immunoblot shows levels of 32 kDa procaspase 3 and its lower molecular weight cleavage products in thalamus cytosolic fractions from homogenates obtained 3, 6, and 24 hr after neonatal hypoxia–ischemia compared with noninjured control samples (SC). Bottom, The corresponding Coomassie-stained blot is shown. Each lane represents a pooled sample of thalamus from three animals at the indicated time point (i.e., sham control and 3, 6, or 24 hr after hypoxia–ischemia).B, Graph represents change in expression of the12 kDa cleavage product in the thalamus over time after neonatal hypoxia–ischemia. Not until 24 hr is there a significant increase in the expression of the 12 kDa fragment. After correcting for protein-loading differences and comparing with control, results are shown as the mean ± SD of four to five pooled samples per time point (*p < 0.05 compared with control).