壳聚糖作载体的NSCs移植对大鼠脑损伤区胶质增生的抑制作用

目的：探讨壳聚糖作载体的神经干细胞（NSCs）移植对大鼠创伤性脑损伤（TBI）区胶质增生的抑制作用。方法：用低温冷冻干燥法制备壳聚糖多孔支架。将从鼠胚前脑中分离的NSCs进行扩增传代。Feeney法制备SD大鼠TBI模型12只，随机均分为2组：损伤对照组和NSCs＋支架移植组2组。术后3个月取脑切片行Nissl染色、GFAP免疫荧光染色，观察两组损伤区和海马变化以及损伤区周边星形胶质细胞增生情况。结果：Nissl染色见损伤对照组创伤区形成烧杯状空洞，损伤侧海马萎缩变形，而NSCs＋支架移植组创伤区有移植物填充且已与宿主整合，损伤侧海马萎缩不明显。GFAP免疫荧光染色，损伤对照组创伤区周边可见到大量GFAP阳性细胞，荧光强度较强，疤痕较宽，而NSCs＋支架移植组创伤区周边仅见到少量的GFAP阳性细胞，荧光强度弱，疤痕较窄。t检验结果显示两组损伤区周围GFAP免疫荧光的灰度值、胶质疤痕宽度有显著性差异（P〈0．01）。结论：大鼠TBI后行壳聚糖作载体的NSCs移植治疗可以抑制脑损伤区胶质增生，从而促进脑损伤的修复。

Depressant Effects of Transplanting NSCs Combined with Chitosan Porous Scaffold on Gliosis at Brain Injured Regions in Rats

Objective： To investigate the effects of transplanting NSCs combined with the chitosan porous scaffold on the reactive gliosis of cerebral cortex with traumatic brain injury （TBI） in rats. Methods： The porous chitosan scaffold was made by using Freezing-drying technique. The NSCs from rat fetal forebrain were cloned and passaged. Sprague-Dawley （SD） rats＇ TBI models were made according to Feeney＇ s method. The TBI rats were randomly divided into injury-control group and NSCs ＋ scaffold group. The rats were immediately debrided after injury, and then NSCs combined with the chitosan porous scaffold were transplanted into injured cerebral cortex in NSCs ＋ scaffold group. Nissl staining and GFAP immunofluorescence techniques were used in brain sections. Results.： A cavity was formed in the ipsilateral injured cortex and the hippocampus were depauperated on Nissl staining slices from injury-control group, in contrast, the hippocampus were not depauperated evidently and there were grafts in the injured cortex on the Nissl staining slices from NSCs ＋ scaffold group. The number and fluorescence intensity of GFAP positive cells near the injured cortex in NSCs ＋ scaffold group were less than that in injury-control group at third month after grafting. The glial scar of cerebral cortex in injury-control group was wider than that in NSCs ＋ scaffold group. Conclusion： Transplanting NSCs combined with the chitosan porous scaffold into the injured cerebral cortex can inhibit the reactive gliosis and promote the recovery after TBI.