骨髓间充质干细胞移植促进脑缺血性损伤大鼠神经细胞黏附分子的表达

背景:骨髓间充质干细胞移植能促进神经功能修复,其作用机制可能与上调神经细胞黏附分子有关。目的:观察骨髓间充质干细胞移植对急性脑缺血损伤大鼠神经细胞黏附分子表达的影响。方法:将SD大鼠按随机数字表法分为假手术组和模型组。模型组大鼠采用线栓法制作大脑中动脉阻塞模型,再随机分为细胞移植组(左侧侧脑室移植同种异体骨髓间充质干细胞5×105)和对照组(移植磷酸盐缓冲液)。假手术组不闭塞大脑中动脉也不移植。结果与结论:移植后7,14d,细胞移植组与对照组梗死灶周围神经细胞黏附分子表达高于假手术组(P<0.01),且细胞移植组高于对照组(P<0.05)。移植后14d,细胞移植组神经功能缺损评分明显低于对照组(P<0.05)。说明骨髓间充质干细胞移植后通过上调局灶性脑缺血大鼠脑梗死灶周神经细胞黏附分子表达促进神经功能的恢复。

Bone marrow-derived mesenchymal stem cell transplantation increased expression of neural cell adhesion molecules in a rat model of ischemic brain injury

BACKGROUND: Studies have demonstrated that transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) improves neurofunctional recovery and the underlying mechanism may be related to upregulated expression of neural cell adhesion molecules. OBJECTIVE: To investigate the effects of BMSC transplantation on the expression of neural cell adhesion molecule after ischemic brain injury in rats. METHODS: Sprague-Dawley rats were randomly divided into a sham-operated group and a middle cerebral artery occlusion (MCAO) group. A permanent focal cerebral ischemia model was established using modified Longa’s method. The MCAO groups were randomly subdivided into a BMSC group (transplantation of 5×10 5 allogenic BMSCs via the left lateral ventricle) and a control group (phosphate buffered saline injection). The sham-operated group received neither MCAO nor BMSC transplantation. RESULTS AND CONCLUSION: At 7 and 14 days following transplantation, neural cell adhesion molecule expression surrounding the infarct foci was significantly higher in the BMSC group and control group (P < 0.01), and the expression in the BMSC group was significantly higher than in the control group (P < 0.05). At 14 days following transplantation, neurological severity score in the BMSC group was significantly lower than in the control group (P < 0.05). BMSC transplantation promoted neurofunctional recovery by upregulating neural cell adhesion molecule expression in the marginal zone of cerebral infarct focus of a rat model of focal cerebral ischemia.