高压氧对脑挫伤大鼠神经行为学和血管内皮生长因子表达的影响

目的 探讨高压氧对脑挫伤大鼠神经行为学和血管内皮生长因子(vascular endothelial growth factor，VEGF)表达的影响。方法 SD大鼠按随机数字表法分为假手术组、脑挫伤组（采用50 9重锤自30 cm处自由落体撞击制备大鼠运动皮质区脑损伤模型）和脑挫伤并高压氧治疗组（高压氧治疗，每天1次，连续7 d），每组10只大鼠。术后7d分别对各组大鼠进行神经损伤严重程度评分（neurological severity scores，NSS），观察动物运动和平衡功能缺损和改进情况。细胞免疫组化方法检测脑组织中VEGF的表达情况。结果 大鼠脑挫伤后出现不同程度抽搐、瘫痪、平衡功能缺失。脑挫伤组NSS评分为(5.6±1.1)分，较假手术组的（0.3±0.1）分明显升高(P＜0.05)；高压氧治疗组NSS功能评分为(3.7±0.7)分，较脑挫伤组明显减少(P＜0.01)。免疫组化染色显示，脑挫伤组VEGF阳性神经元数为(15±3)个，较假手术组(27±2)个明显减少(P＜0.05)；高压氧治疗组VEGF阳性神经元数为(2l±2)个，较脑挫伤组明显增加(P＜0.05)。结论高压氧治疗能有效促进脑挫伤大鼠神经功能恢复，其作用机制可能与VEGF的增加有关。

Effects of hyperbaric oxygen on neurological behavior and VEGF expression in rats following traumatic brain injury

Objective To explore the effects of hyperbaric oxygen on neurological behavior and vascular endothelial growth factor (VEGF) in rats with traumatic brain injury (TBI). Methods Thirty rats were randomly divided into three groups, ie, control group, TBI group ( a 50 g weight-drop device was employed and fell from 30 cm height to induce the injury) and hyperbaric oxygen group ( HBO group,treated with hyperbaric oxygen once per day for seven days after TBI), 10 rats per group. Neurological severity score (NSS) was used to evaluate the movement and balance impairment in all groups. Expression of VEGF was detected by means of immunocytochemical staining.Results After TBI, the rats presented different degrees of convulsions, paralysis and balance dysfunction. The NSS score was (5.6 ±1.1 ) points in the TBI group and (0.3 ± O. 1 ) in the control group, with statistical difference ( P ＜0.05). While NSS score was (3.7 ± O. 7) points in the HBO group, showing a significant decrease compared with that in the TBI group (P ＜ 0. O1 ). Immunohistochemical staining showed 15 ± 3 positive neurons of VEGF in the TBI group, significantly less than 27 ± 2 in the control group ( P ＜ 0.05 ). There were 21 ±2 positive neurons of VEGF in the HBO group, significantly less than 21 ±2 in the TBI group (P ＜0.05). Conclusion Hyperbaric oxygen may attenuate experimental traumatic brain injury by stimulating production of VEGF.