The Study Of Neurogenesis, Basic Fibroblast Growth Factor Expressing And The Relationship Between Them After Transient Focal Cerebral Ischemia In Rat

To investigate the time regulation of the neurogenesis in subventricular zone(SVZ) and subgranular zone(SGZ) and the expression of basic fibroblast growth factor (bFGF) after the transient focal cerebral ischemia, and analyse the relationship between neurogenesis and bFGF expressing.Materials and methods: The right middle cerebral artery of rats were occluded (MCAO) for 60 minutes to establish transient focal cerebral ischemia model. Using BrdU to label the S phase cells of SVZ and SGZ, hematoxylin and eosin (FIE) staining and immunohistochemistry methods to observe neural necrosis, BrdU-labled positive cells (ld, 4d, 7d, 10d, 14d after ischemia) and the expression of bFGF (6h, 12h, 24h, 2d, 5d, 8d, 1 ld, 15d after ischemia). Count the positive cell's area, use ANOVA to analyse the difference of different group and compare the relationship between BrdU and bFGF.Results: 1. All the rats of experimental groups circled to the contralateral side of ischemia after the operation, neural necrosis could be observed in caudoputamen 12h after transient focal ischemia, and increased 24h after ischemia. At 5d, the caudoputamen and parietal cortex of the ischemic side shrinked sharply and then liquefied 8d after ischemia. The abnormal cells of hippocampal Cornu Ammon second area (CA2) could be observed 5d after ischemia and markedly increase at 8d, these meant that the transient focal cerebral ischemia model was established successfully. 2. Neurogenesis increased obviously in ipsilaterial SVZ of the ischemic side and with a peaked 7d after ischemia. At the same time theBrdU-labled cells in the contralateral SVZ increased too, but the degree were less than the ischemic side and with a peak l0d after ischemia, both start to decrease after that in the two sides. We haven't observed BrdU-labled positive cells increasing in SGZ. 3. The expression of bFGF increased in many cerebral area after ischemia, in the ipsilateral SVZ, the bFGF's expressing start to increase at 12h and with a peak at 24h, then start to decrease, there is a similar increasing in the contralateral SVZ. We also observed the increasing expression of bFGF at CA2 of hippocampus 5d and with a peak 8d after ischemia, and there is a slightly increasing of bFGF in the contralateral side.Conclusions: Neurogenesis increased in SVZ and was related to the increasing expression of bFGF after transient focal cerebral ischemia. bFGF has both protective effect to neuron and increasing neurogenesis .