Fig. 5

A protective role for cortisol in TBI pathogenesis. a Histologic examination of normal control and injured brain at 7 days after TBI with or without administration of S1P or rolipram. The impact site was pointed by an arrow. The region of the cerebral cortex was highlighted in a dashed black line square and enlarged in panel (b); and the hippocampus was outlined by a dashed white line square and magnified in panel (c). Representative results of six mice in each group. d Representative immunofluorescence results of anti-CD3 antibody staining at hippocampus beneath the injured site and enlarged in panel (e). f Representative immunofluorescence staining for Caspase-3 expression at hippocampus beneath the injured site. g Representative TUNEL staining for apoptosis cells at the injury site. Percentages of CD3-positive cells in panel (e), Caspase-3-positive cells in panel (f), and optical density of TUNEL staining in panel (g) were determined by ImageJ and expressed as means ± SEM in (h), (i), or (j), respectively. n = 6, significance was measured using one-way ANOVA. *P < 0.05, **P < 0.01, ***P < 0.001 and NS, no significance compared between indicated groups. The experiment was repeated three times with similar results