Abstract:OBJECTIVE: To explore the protective mechanism after hypoxic-ischemic and reperfusion damage of the brain. METHODS: Seven-day-old SD rats from seven broods (eight rats from each brood, n = 56) were randomly divided into the HIBD group and sham operation group. The HIBD model was established by temporarily occluding the right common carotid artery for 3 hours with a thread through an elastic tube, and then they were exposed to the gas mixture of 80 ml/L oxygen and 920 ml/L nitrogen for 1 h. After 3 hs, the common carotid artery was reperfused. The blood flow of the right common carotid artery was detected by the Color Doppler. The expressions of p-CREB and c-fos in the hippocampus at different reperfusion periods (3 hs, 6 hs, 24 hs, 48 hs, 72 hs and 7 days after reperfusion and 24 hs after sham operation) were detected by immunohistochemical methods. Thionin staining was used to observe the apoptosis of neurons. RESULTS: In the HIBD group, the expression of p-CREB in the right hippocampus peaked 3 hs and 24 hs after reperfusion, and then decreased to the level of the sham group on the seventh day. The expression of c-fos reached the peak 6 hs after reperfusion, and another peak appeared 48 hs after reperfusion. Seven days after reperfusion, the number of c-fos positive cells decreased, but they were still more than those in the sham operation group ( P <0.0l). Using Thionin staining, we found that the apoptosis of neurons in the CA1 region marked 24 hs after reperfusion. CONCLUSIONS: The persistent activation of CREB in the hippocampus regulates the expression of c-fos through signal transduction, and it is involved in the course of neurons' survival and repair during the period of post hypoxic-ischemia reperfusion. It is very important for the protection of pyramidal hippocampal neurons of the damaged side, especially of the sensitive CA1 region. [Chin J Contemp Pediatr, 2003, 5(1): 12 - 16]
