CAJ | 학술논문

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。
목적 탐토고압양대뇌좌상대서신경행위학화혈관내피생장인자(vascular endothelial growth factor，VEGF)표체적영향。방법 SD대서안수궤수자표법분위가수술조、뇌좌상조（채용50 9중추자30 cm처자유락체당격제비대서운동피질구뇌손상모형）화뇌좌상병고압양치료조（고압양치료，매천1차，련속7 d），매조10지대서。술후7d분별대각조대서진행신경손상엄중정도평분（neurological severity scores，NSS），관찰동물운동화평형공능결손화개진정황。세포면역조화방법검측뇌조직중VEGF적표체정황。결과 대서뇌좌상후출현불동정도추휵、탄탄、평형공능결실。뇌좌상조NSS평분위(5.6±1.1)분，교가수술조적（0.3±0.1）분명현승고(P＜0.05)；고압양치료조NSS공능평분위(3.7±0.7)분，교뇌좌상조명현감소(P＜0.01)。면역조화염색현시，뇌좌상조VEGF양성신경원수위(15±3)개，교가수술조(27±2)개명현감소(P＜0.05)；고압양치료조VEGF양성신경원수위(2l±2)개，교뇌좌상조명현증가(P＜0.05)。결론고압양치료능유효촉진뇌좌상대서신경공능회복，기작용궤제가능여VEGF적증가유관。
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.