| Objective: The neuron apoptosis and expression of Fas protein and caspase-8 protein were observed dynamically in rats' cortex and hippocampus CA1 region following ischemic-preconditioning and Sodium Ferulate combined with ischemic-preconditioning, the possible mechanism of the delayed neuronal apoptosis after ischemic- preconditioning was discussed preliminary.Matericals and Methods: Global ischemia in 120 Wistar rats was established by obstructing four blood vessels. All rats were divided randomly into sham(S) group(n=15), preconditioning(P) group(n=15), ischemia preconditioning (IP) group(n=30), cerebral ischemia (I)group(n=30) and Sodium Ferulate (SF) group(n=30). Neuronal apoptosis, Fas and caspase-8 proteins expression at 6h, 12h, 24h and 48h after global ischemia in IP group, I group and SF group were detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling(TUNEL) and immunohistochemistry methods, the survival neurons in cortex and hippocampus CA1 region of all groups was detected at 48h, 7d and 12w after global ischemia by Nissl body staining.Results: 1. Neurons at 48h, 7d and 12w after global ischemia were 250±36.9, 265±18.3 and 267±9.6 in S group, 249±10.5, 277±11.1 and 222±7.5 in P group respectively, there was no significant difference between two groups. Neurons survived in IP group(268±8.5) and in SF group(244±12.5) were compared with that in sham group(265±18.3) and no significant difference(P>0.05) were found, but they were higher than that in I group significantly(135±5.6 p<0.001)at 7 days after global ischemia. Compared with that in S group(267±9.6)at 12 weeks after global ischemia, neurons lost notability in IP group(30±3.7), SF group (22±2.7) (P<0.01), but there were no significant difference when both of them were compared with that in I group(19±2.8).2. At 48 hours after ischemia a little expression of Fas protein and faint immunoreaction intensity were observed in S group(97.7±11.6, 146±2.5), and they were 101.2±8.8 and 139±1.9 respectively in P group in CA1 region. At 6h after ischemia, Expression of Fas protein(213.8±42.6) and immunoreaction intensity (132±8.1) increased throughout the whole brain including cerebral cortex and hippocampus in I group, they reached the peak at 12h(380.8±48.2,121±3.8) and began to decrease at 24h (175.0±40.7,129±7.7) after ischemia. The number of neuron with expression of Fas protein and immunoreaction intensity increased at 12h(192.8±35.3, 134±6.6) and reached the peak at 24h (266.3±12.9,126±2.2), began to decrease at 48h(121.5±28.9, 142±3.0)after ischemia in IP group. Compared to I group the expression of Fas protein was delayed, but the peak number in IP group was significant less than that in I group(266.3±12.9,380.8±48.2　p<0.01). In SF group, the cell number with expression of Fas protein and the immunoreaction intensity increased at 12h(178.5±35.8, 137±5.2)and reached the peak at 24h (249.6±21.3, 128±6.1), began to decrease at 48h (127.1±19.5, 140±2.6)after ischemia. Compared to I group the expression of Fas protein was delayed, the peak number in SF group was significant less than that in I group(249.6±21.3,380.8±48.2　p<0.01), but no significant difference was found between IP group and SF group(249.6±21.3,266.3±12.9　p>0.05).3. At 48h after ischemia a little expression of caspase-8 protein and faint immunoreaction intensity were observed in the sham group(19.8±8.8, 152±1.6)and they were 22.9±5.9 and 151±2.8 respectively in P group in CA1 region. At 6h after ischemia, the expression of caspase-8 protein increased(154.2±18.4) in cells and detected throughout the cerebral cortex and hippocampus in I group, reached the peak at 12h(222.8±17.1), began to decrease at 48h(222.8±17.1) after ischemia; the immunoreaction intensity began to increase at 6h(142±9.0), reached the peak at 12h(137±11.1)and elevated persistently till 48h(134±5.3) after ischemia. In IP group, the cell number with ex...
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