| The morbidity of ischemic cerebral vascular diseases is increasing gradually, and this kind of diseases attracts more and more attention because of its threat against the health and lives of human beings. For the known remedies have not acquired perfect effects on many patients, how to improve the injured neurological functions of the patients suffering from cerebral ischemia is still the key problem of the present time. Recently, that NSCs are discovered in the brains of adult mammalian throws some light on the treatment of CNS diseases. The discovery of NSCs suggests self-repair of the brain. After cerebral injuries, activation of endogenous neural precursor cells contributes to the recovery of injured neurological functions. In addition, the transplantation of exogenous NSCs can also be use to improve the neurological functions, but the limited resources confine the application of NSCs. BMSCs are multipotential and can be obtained from the bone marrow, and these properties make them meet the basic requirements of "seed cells". Based on above points, the analysis of the activation of endogenous neural precursor cells and application of NSC and BMSC transplantation to cerebral ischemia will make a significant theoretical contribution to therapeutic strategies of cerebral ischemia.Part I The Activation of Endogenous Neural Precursor Cells after FocalCerebral Ischemia of RatsObjective: The present study aimed to explore the activation of endogenous neural precursor cells and neurogenesis in different brain regions at different time points, and then to further clarify the mobilizing process of self-repair, so that theoretical assistance for clinical therapy of cerebral ischemia could be provided.Methods: Focal cerebral ischemia was induced by transient MCAo with a monofilament suture in adult Wistar rats, which were assesssed and killed at 3, 7, 14, 21 days after focal cerebral ischemia. BrdU was injected intraperitoneally every 12h for 2 days to label dividing cells of the above ischemic rats, normal and sham-operated rats 3 days before sacrifice, and these rats were killed at 1 day after the last injection. The scores of neurological deficits were used as a general assessment of cerebral ischemia. Microscopy, Evans Blue and TTC staining wereemployed to observe the position and area of cerebral ischemia. Nestin and BrdU were detected by immunohistochemistry, and measurement of nestin, NSE and GFAP mRNA in brain tissue were through RT-PCR. These results made us able to analyze the activation of endogenous precursor cells and neurogenesis after cerebral ischemia.Results: (1) Left hemiplegia and right Hornor's sign were observed after transient right MCAo with a monofilament suture. Evans Blue, TTC and HE staining showed that ischemic regions were located hi right striatum and frontoparietal cortex. The position and area were stable at each time. (2) In normal rats, nestin-positive cells were present in SVZ of the lateral ventricle and DG of the hippocampus. After focal ischemia, the numbers of nestin-positive cells hi above two regions increased markedly with a peak at 7 days after ischemia compared with normal rats. However, the increase in the number of nestin-positive cells in DG was less obvious than that in SVZ. Numerous nestin-positive cells were also observed hi the ischemic and surrounding regions with a peak at 7 days after ishchemia. Although with a consistent variation trend, a significant increase in the number of nestin-positive cells was found in the ischemic hemisphere compared with the contralateral homologous tissue. (3) In normal rats, BrdU-positive cells present in SVZ of the lateral ventricle and DG of the hippocampus were less than the cells positive for nestin. After focal cerebral ischemia, the numbers of BrdU-positive cells in above two regions increased markedly with a peak at 7 days after ischemia compared with normal rats. However, the increase in the number of BrdU-positive cells in DG was less obvious than that in SVZ. Numerous BrdU-positive cells were also observed...
|
PDF Full Text Request