骨髓间充质干细胞移植影响慢性脑缺血大鼠认知功能及海马区Nogo-A、NgR的表达

Transplantation of bone marrow mesenchymal stem cells improves cognitive function of rats with chronic cerebral ischemia and decreases Nogo-A and NgR protein expression in the hippocampus

背景:骨髓间充质干细胞移植可降低脊髓损伤及脑梗死大鼠的Nogo-A及NgR的表达。目的:观察骨髓间充质干细胞移植对慢性脑缺血大鼠认知功能及海马区Nogo-A及NgR蛋白的表达。方法:将30只SD大鼠随机等分为假手术组、模型组及骨髓间充质干细胞组,后2组采用双侧颈总动脉永久结扎法建立大鼠慢性脑缺血模型,骨髓间充质干细胞组在建模7d后尾静脉注射移植用ficoll密度梯度离心法分离培养大鼠骨髓间充质干细胞1×107个。结果与结论:与假手术组比较,模型组大鼠平均逃避潜伏期明显延长(P<0.01),穿过原平台位置次数明显减少(P<0.01),海马中Nogo-A与NgR蛋白表达明显增加(P<0.05);而与模型组比较,骨髓间充质干细胞组大鼠平均逃避潜伏期明显缩短(P<0.01),穿过原平台位置次数明显增加(P<0.05),海马组织中Nogo-A及NgR表达明显减少(P<0.05)。说明骨髓间充质干细胞移植具有保护慢性脑缺血大鼠空间学习与记忆能力的作用,其作用可能与降低Nogo-A及NgR蛋白表达有关。

BACKGROUND：Transplantation of bone marrow mesenchymal stem cells can decrease Nogo-A and NgR expression in rats with spinal cord injury and cerebral infarction.OBJECTIVE：To investigate the effects of transplantation of bone marrow mesenchymal stem cells on cognitive function of rats with chronic cerebral ischemia and Nogo-A and NgR protein expression in the hippocampus.METHODS：Thirty Sprague-Dawley rats were randomly divided into sham-surgery,model and bone marrow mesenchymal stem cells groups.Rats in the latter two groups were established into model of chronic cerebral ischemia by permanent ligation of bilateral common carotid artery.In the bone marrow mesenchymal stem cells group,at 7 days after chronic cerebral ischemia induction,bone marrow mesenchymal stem cells（1×107） isolated by ficoll density gradient centrifugation were transfused into rats via the tail vein.RESULTS AND CONCLUSION：Compared with sham-surgery group,the average escape latency was significantly shortened（P 0.01）,the number that rats passed through the platform was significantly increased（P 0.05）,and Nogo-A and NgR expression in the hippocampal tissue was significantly decreased（P 0.05） in the bone marrow mesenchymal stem cells group.These findings suggest that transplantation of bone marrow mesenchymal stem cells protects spatial learning and memory abilities of rats with chronic cerebral ischemia.This effect is possibly related to decreased Nogo-A and NgR protein expression.