摘要
为观察脑缺血后神经元特异性烯醇化酶 (NSE)活性的动态变化以及高压氧 (HBO)治疗对其的影响 ,并探讨高压氧的治疗机制 ,将SD大鼠随机分为缺血再灌注组 (I/R)、高压氧处理组 (HBO)及假手术组。以四动脉阻断法建立脑缺血再灌注动物模型 ,缺血 2 0min。分别于再灌注 6、2 4、4 8及 96h取血 ,用酶联免疫吸附法 (ELISA)测定血浆中的NSE活性。结果显示各I/R组血浆NSE活性较假手术组均有升高 ,其中 6h及 96hI/R组与假手术组相比差异有显著性意义 (P <0 .0 5)。提示 :缺血再灌注损伤导致血浆NSE活性升高 ,I/R组的NSE活性出现 6h和 96h时的 2次升高 ,可能与脑缺血过程中出现的急性神经元坏死及其后的迟发性神经元凋亡相关。各HBO治疗组与相应时间点I/R组相比 ,6hHBO组的NSE活性较 6hI/R组显著降低 (P <0 .0 5) ,其他时间点HBO治疗组与相应I/R组相比无显著性差异 (P >0 .0 5)。提示 :HBO治疗作用表现为NSE活性的恢复比同时相点I/R组快 ,本研究中
The aim was to observe the dynamic change of neuron-specific enolase activity a fter experim ental cerebral ischemia and the effect of hyperbaric oxygen (HBO) on it, and exp lore the mechanism of HBO therapy. Sprague Dawlay rats were randomly divided int o three groups: ischemia/reperfusion group (I/R), group treated by HBO (HBO) and sham operated group (Sham-O) as control. Global brain ischemia was induced usi ng a modified four-vessel occlusion model originally described by Pulsinelli an d Buchan. Blood was collected in EDTA respectively at reperfusion time of 6th h, 24th h, 48th h and 96th h after 20 min of ischemia, the NSE activity was measur ed by ELISA. The plasma NSE levels on 6th h and 96th h I/R groups were significant ly h igher than Sham-O group ( P <0.05). These data suggest that plasma NSE increa sed after global ischemia/reperfusion. The increment of 6th h and 96th h presuma bly represented the acute neuronal necrosis and delayed neuronal death respectiv ely. Compared with 6th h I/R group, the NSE level on 6th h HBO group significantly de crea sed ( P <0.05). There were no statistically significant differences between ot her HBO groups and corresponding I/R groups ( P >0.05). These data indicate th at the recovery of NSE level in HBO group is earlier than I/R group. The optimal therapeutic window of HBO in this study is 6 h after reperfusion.
出处
《首都医科大学学报》
CAS
2004年第1期19-22,共4页
Journal of Capital Medical University
基金
北京市教委科技发展计划基金(0 0KJ10 8)资助项目
关键词
高压氧
大鼠
脑缺血
神经元特异性烯醇化酶
hyperbaric oxygen
cerebral ischemia
reperfusion
neuron-specific enolase
apoptosis
