鼠脑梗死后自体神经干细胞的原位增殖、分化及其可塑性

目的研究成年大鼠脑梗死后自体神经干细胞的原位增殖、分化及其可塑性。方法雄性Wistar大鼠共90只,分对照组(n=10)、脑梗死后1d组(n=16)、脑梗死后3d组(n=16)、脑梗死后7d组(n=16)、脑梗死后14d组(n=16)、脑梗死后28d组(n=16)。用免疫组织化学方法动态检测BrdU、GFAP、NeuN、PSA-NCAM的表达。BrdU确定神经干细胞的增殖,GFAP、NeuN确定神经干细胞的分化,PSA-NCAM确定神经干细胞的可塑性。结果与对照组相比,大鼠海马BrdU 细胞数在脑梗死后1d组开始增加,7d组达到高峰,28d组接近正常水平;BrdU /GFAP 细胞数在脑梗死前后无明显变化;BrdU /NeuN 细胞数在脑梗死后14d组开始增加,28d组最多;BrdU /PSA-NCAM 细胞数在脑梗死后7d组开始增加,14d组达到高峰,28d组开始下降,但仍高于对照组,大约占同期BrdU阳性细胞数60%。结论大鼠脑梗死激活自体神经干细胞原位增殖,大多数增殖的神经干细胞分化成神经元并且具有可塑性。

Proliferation,differentiation and plasticity of neural stem cells in adult rats after cerebral

Objective To investigate the proliferation,differentiation and plasticity of neural stem cells in adult rats after cerebral infarction. Method Brain infarction models of rats were made and the dynamic expression of bromodeoxyuridine(BrdU), glial fibrillary acidic protein(GFAP), neuronal nuclear antigen (NeuN)and polysialylated neural cell adhesion molecule(PSA-NCAM)were determined by immunohistochemistry and immunofluorescence staining. BrdU was used to mark dividing neural stem cells. GFAP and NeuN were used to mark differentiating neural stem cells. PSA-NCAM was used to determine plasticity of proliferating neural stem cells in situ. Results Compared with the controls, the number of BrdU-labeled cells increased strikingly at 1 day, approximately six fold with a peak at 7 day, markedly decreased at 14 day ,but it was still elevated compared with that of the controls, nearly remained unchanged at 28 day. The number of BrdU-labeled with GFAP-positive cells nearly remained unchanged in the hippocampus after cerebral infarction. The number of BrdU-labeled with NeuN-positive cells increased strikingly at 14 day, reached maximum at 28 day in the hippocampus after cerebral infarction in rats. The number of BrdU-labeled with PSA-NCAM-positive cells increased strikingly at 7 day, reached maximum at 14 day, markedly decreased at 28 day, was equal to 60% of the number of BrdU-positive cells in the same period. Conclusion Our results indicate that cerebral infarction stimulated the proliferation of inherent neural stem cells and most proliferated neural stem cells differentiated into neurons and represented neural plasticity.