大鼠创伤性脑损伤后脑组织ICAM-1及血糖变化与细胞凋亡的实验研究

The relationship of ICAM-1 and changes in blood glucose and cell apoptosis after traumatic brain injury in rats

目的研究大鼠创伤性脑损伤后脑组织ICAM-1和血糖变化与神经细胞凋亡的关系。方法采用大鼠自由落体脑损伤模型(Feeneys model),分别在伤后6、24、72、168h免疫组织化学检测ICAM-1、Hoechst染色定量凋亡细胞;测定伤前0.5h及伤后6、12、24、48、72、120、168h各组动物的血糖值。结果脑损伤程度越重,ICAM-1的IOD值、血糖浓度和神经细胞凋亡的个数升高的速度越快、峰值越高;神经细胞凋亡的个数从伤后6h即明显高于对照组,并持续增高。结论创伤性脑损伤后早期神经细胞凋亡可能与ICAM-1介导的细胞黏附及升高血糖的胰高血糖素、糖皮质激素等介导的细胞凋亡有关。

Objective To study the relationship of ICAM-1 and changes in blood glucose and cell apoptosis after traumatic brain injury in rats. Methods Based upon the Feeney＇s model, Intercellular adhesion molecule 1 （ ICAM-1 ） and Cell apoptosis of each animal group were measured 6,24,72,168 hours after the injury. The blood glucose concentration of each animal group were measured at half on hour hour before the injury and 6,12,24,48,72,120,168 hours after the injury. Results The severer the trauma was, the faster the blood glucose concentration and the IOD of ICAM-1 and the number of cell apoptesis increased. The number of cell apoptesis increased markedly at 6 hours after the injury, and increased continually. Conclusion The over expression of ICAM-1 and that which increased blood glucose concentration such as glucagons and cortisol may be the cause of inducing cell apoptosis.