| 摘要: |
| 目的探讨慢性酒精暴露对SD大鼠急性脑缺血再灌注后早期海马齿状回颗粒下区（SGZ）神经干细胞（NSCs）的影响。方法将SD大鼠随机分为正常组（自来水喂养）、对照组[单纯大脑中动脉闭塞（MCAO），自来水喂养]和酒精组（酒精暴露后MCAO，6%乙醇水溶液喂养）。正常组于饲养28d后灌注取脑，对照组、酒精组分别于造模后1、3、7d灌注取脑。切取以视交叉前缘至垂体后缘包含海马区厚约4mm的组织块进行石蜡包埋、切片、HE染色、巢蛋白（Nestin）染色处理；使用图像分析系统采集图像，计算并比较每张切片Nestin阳性细胞数。结果HE染色可见对照组、酒精组造模后1d脑组织开始出现神经元损伤，造模后3d达到高峰，造模后7d开始恢复，且酒精组更为严重；正常组未见神经元损伤。Nestin染色可见对照组造模后1dSGZNestin阳性细胞开始增多，造模后7d达到高峰；酒精组造模后1dSGZNestin阳性细胞开始增多，3d达到高峰，造模后7d明显回落；正常组SGZ可见少量散在分布的Nestin阳性细胞。酒精组Nestin阳性细胞的数量明显少于对照组（P＜0.05）。结论慢性酒精暴露可明显抑制MCAO后早期内源性NSCs增殖，抑制损伤后神经组织自身的修复，从而导致缺血性脑卒中的预后不良。 |
| 关键词: 慢性酒精暴露 大脑中动脉闭塞 神经干细胞 |
| DOI： |
| 分类号: |
| 基金项目: |
|
| Effect of chronic alcoholic exposure on endogenous neural stem cells in rat hippocampal dentate gyrus at early stage of acute cerebral ischemia and reperfusion |
|
CHEN Zhongliang, LI Zhengyi, LI Honglei
|
|
Huzhou Central Hospital
|
| Abstract: |
| Objective To investigate the effect of chronic alcoholic exposure on the proliferation of endogenous neural
stem cells (NSCs) in rat subgranular zone (SGZ) in hippocampal gyrus at the early stage of acute cerebral ischemia and reperfusion. Methods Forty-two SD rats were divided into 3 groups randomly: 6 rats were fed with clean water (normal group), 18 rats underwent middle cerebral artery occlusion (MCAO) /reperfusion and fed with clean water (model group) and 18 rats underwent MCAO/reperfusion and fed with 6% alcoholas (alcohol group). Rats from normal group were sacrificed 28 days after feeding, and rats from model group and alcoholic group were sacrificed at 1, 3 or 7 days after establishment of MCAO and reperfusion model, respectively. Brain samples were collected immediately after sacrifice. Brain tissues including hippocampal dentate gyrus were selected for paraffin imbedding and tissue slicing. HE stain was performed to detect the neuron damage, and immunohistochemistry stain was applied to detect the expression of Nestin in brain tissue. Images were obtained by image analysis system and the number of Nestin positive cells in each slice was calculated. Results Based on the HE stain, neuron damage was observed from day 1 after model establishment in model group and alcoholic group, peaked at the day 3 and reduced at the day 7. Neuron damage was not observed in normal group. A few Nestin positive cells were detected in the SGZ of normal group from the immunohistochemistry. In model group, the number of Nestin positive cells increased from day 1 after model establishment, peaked at day 7. And in alcoholic group, the number of Nestin positive cells increased from day 1 after model establishment, peaked at day 3, and reduced at day 7. Compared with model group, the number of Nestin positive cells in
SGZ of alcoholic group was significantly reduced (P＜0.05). Conclusion Chronic alcoholic exposure can reduce the proliferation
of endogenous NSCs in SGZ, leading to a poor prognosis of cerebral ischemic/reperfusion injuty. |
| Key words: Chronic alcoholic exposure Middle cerebral artery occlusion Neural stem cells |
