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目的观察大鼠局灶性脑缺血再灌注后神经细胞黏附分子-43(NCAM)和生长相关蛋白(GAP-43)基因表达在神经功能恢复过程中的作用。方法应用线栓法建立大鼠大脑中动脉阻塞(MCAO)再灌注模型。采用Bederson神经功能评分法评价脑缺血90min再灌注2h、12h、1d、2d、3d、7d和14d等时间点大鼠神经功能情况,采用原位杂交技术检测NCAMmRNA和GAP-43mRNA的表达。结果大鼠脑缺血再灌注后,神经功能评分于再灌注2d开始降低,神经功能逐渐恢复。在皮质区和纹状体区,脑缺血侧GAP-43mRNA表达于再灌注12h和2d出现峰值,以后逐渐降低,至14d恢复至假手术组水平。皮质区NCAMmR-NA的表达于再灌注2h后开始增强,12h后达高峰;纹状体区NCAMmRNA的表达于再灌注后2h时开始增强,1d后达高峰,以后逐渐减少,14d降至基础水平。结论脑缺血再灌注后,NCAM的表达可能参与了脑细胞的修复过程,GAP-43mRNA的表达增强可能与损伤神经的功能恢复有关。
Objective To observe the role of neural cell adhesion molecule-43 (NCAM) and growth-associated protein (GAP-43) gene expression in the recovery of neural function after focal cerebral ischemia-reperfusion in rats. Methods The rat model of middle cerebral artery occlusion (MCAO) reperfusion was established by thread occlusion. Bederson neurological score was used to evaluate the neurological function of rats at 90 min after cerebral ischemia and 2h, 12h, 1d, 2d, 3d, 7d and 14d after reperfusion. The expression of NCAMmRNA and GAP-43mRNA were detected by in situ hybridization. Results After cerebral ischemia-reperfusion in rats, the neurological function score decreased at 2d after reperfusion, and the neurological function recovered gradually. In the cortical and striatum regions, the expression of GAP-43mRNA on the ischemic side of cerebral cortex peaked at 12h and 2d after reperfusion, then decreased gradually and returned to sham-operated group level on the 14th day. The expression of NCAMmR-NA in cortex began to increase at 2h after reperfusion and peaked at 12h. The expression of NCAMmRNA in striatum began to increase at 2h after reperfusion and peaked at 1d, then decreased gradually and dropped to the basal level at 14d . Conclusion The expression of NCAM may be involved in the repair process of brain cells after cerebral ischemia and reperfusion, and the increased expression of GAP-43 mRNA may be related to the functional recovery of injured nerve.