摘要
目的观察不同时间窗高压氧治疗(HBOT)对脑缺血-再灌注(I/R)损伤后学习记忆功能的影响,探讨其可能的机制。方法制备大鼠可逆大脑中动脉阻塞脑损伤模型。分别于再灌注后6及24h起始HBOT,观察空间学习记忆功能,计算梗死百分比,免疫组化检测鼠脑iNOS、ChAT,及Bcl-2、Bax表达阳性神经元。结果与缺血对照组比较,早期治疗组大鼠学习记忆功能显著改善;脑梗死比率显著缩小(P<0.01);海马CA1区ChAT阳性神经元增多,iNOS表达减少,且Bcl-2表达增多(均P<0.01),Bax阳性神经元数无明显变化。晚期治疗组显示与早期治疗组改变相似,但iNOS、Bax表达无明显差异。结论早期或延迟HBOT均可改善大鼠脑I/R损伤引起的学习记忆功能不良,显示有神经保护作用。
Objective To investigate the effect of hyperbaric oxygen therapy （HBOT） at different time windows on learning and memory function of model rats with ischemia-reperfusion （IR） injury and to explore its possible neural protective mechanism. Methods Focal cerebral IR injury rats model was induced by reversible middle cerebral artery occlusion （MCAO）. HBOT was administered at 6 or 24 hours after reperfusion respectively to observe the spatial learning and memory abilities and measure the infarct volume ratio and positive neurons of iNOS, CHAT, Bcl-2, Bax proteins in hippocampal CA1 region by immunohistochemistry. Results The learning and memory abilities improved and the brain infarct volume ratio diminished markedly （P 〈 0. 01 ）, the positive neurons of CHAT increased, iNOS expressions decreased and Bcl-2 positive neurons increased significantly （ all P 〈 0. 01 ）, but Bax expression had no obvious changes in hippocampal CA1 region in the early HBOT group comparing to those in ischemia-control group. Similar changes occurred in delayed HBOT group, but the number of reaction positive neurons of iNOS and Bax had no significant difference. Conclusions Both earlier and delayed HBOT could play neural protective effect against transient MCAO induced long-term brain morphological and histological deficits and spatial learning and memory dysfunction.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2007年第15期1447-1449,共3页
Chinese Journal of Gerontology
关键词
大脑中动脉阻塞
缺血-再灌注损伤
高压氧
学习记忆功能
Middle cerebral artery occlusion （MCAO）
Reperfusion injury
Hyperbaric oxygen
Learning and memory
