摘要
目的探讨高压氧（HBO）对缺氧缺血性脑损伤（HIBD）新生大鼠海马CA3区神经元突触超微结构和突触素（p38）表达的影响。方法按Bjelke法制作HIBD新生大鼠动物模型，随机分为HIBD组、HIBD＋HBO组、单纯HBO组和对照组四组，每组10只。HBO组大鼠于术后24h开始给予2ATA的高压氧治疗，1h／d，持续14d。于大鼠4周龄时采用水迷宫试验检测各组大鼠的学习记忆功能，而后取大鼠海马组织通过透射电镜观察各组海马CA3区锥体神经元超微结构，免疫组化和图像分析技术检测p38的表达。结果HIBD组大鼠学习记忆能力[（15．5±4．9）次]明显低于对照组[（10．6±3．4）次]（P〈0．01），经HBO干预后，测试成绩明显提高[（11．3±2．6）次]，与对照组间差异无统计学意义（P〉0．05）。与对照组比较，HIBD组海马CA3区锥体细胞见部分核膜消失、线粒体嵴模糊、神经元突触间隙增宽，突触前囊泡减少，突触后致密物变薄；HIBD＋HBO组神经元和突触无明显异常。HIBD组海马CA3区始层、辐射层、腔隙分子层及齿状回分子层突触素光密度值（0．41±0．19、0．21±0．11、0．08±0．03、0．38±0．16）明显低于HIBD＋HB0组（0．77±0．17、0．67±0．16、0．46±0．13、0．864-0．14）和对照组（0．82±0．16、0．70±0．16、0．53±0．15、0．91±0．17）（P〈0．01），而HIBD＋HBO组和对照组差异无统计学意义（P〉0．05）。结论高压氧发挥治疗作用的机制可能与阻止或减轻HIBD后突触超微结构的损伤、促进突触的重建有密切关系。
Objective To observe the effects of hyperbaric oxygen （HBO） on synaptic ultrastructure and the synaptophysin expression （p38） in hippocampal CA3 after hypoxia-ischemic brain damage （H1BD） in neonatal rats. Methods The rat model of HIBD was made by the method of Bjelke and divided randomly into two groups （ n = 10 ） --HIBD group and HBO-treated HIBD group. Another 20 rats underwent sham-operation and were also divided randomly into HBO-treated control group and the control group. After 24 h of the operation,the rats of the HBO-treated groups received HBO （2ATA, 1 h/d） for 14 days. When rats were 4 weeks old, the learning-memory ability of rats in every group was evaluated through water-maze test. Their hippocampal ultrastructure was observed with electron microscope and the p38 expression was detected immunohistochemieally. Results Compared with the control group [ （ 10. 6 ± 3.4） times], the water-maze learning ability of the rats in HIBD group [ （ 15.5 ±4. 9） times] was significantly decreased（P 〈 0.01 ）, while the learning-memory ability of the HBO-treated HIBD group [ （ 11.3 ± 2. 6 ） times ] was significantly improved. There was no significant difference in the water-maze test between the HBO-treated HIBD group and the control group （P 〉 0. 05 ）. Compared with the control group, the ultrastructure of pyramidal neuron of hippocampal CA3 was distorted in HIBD group under the electron microscope. Compared with that in HBO-treated HIBD group （0.77 ± 0. 17, O. 67 ± 0. 16, 0.46 ± 0. 13, 0. 86 ±0. 14） and the control group （0. 82 ±0. 16, 0. 70 ±0. 16, 0. 53 ±0. 15, 0.91 ±0. 17）, the corrected optical densities （COD） of immunoreactive products of the hippocampal CA3 p38 were significantly decreased in HIBD group （0. 41 ±0. 19, 0. 2l ±0. 11, 0. 08 ±0. 03, 0. 38 ±0. 16） （P 〈0. 01 ）. There was no significant difference in either ultrastructure or immunohistochemically reactive COD of p38 between the HBO-treated HIBD group and the control grou
出处
《中华儿科杂志》
CAS
CSCD
北大核心
2010年第3期199-203,共5页
Chinese Journal of Pediatrics
关键词
缺氧缺血
脑
高压氧
突触囊泡蛋白
显微镜检查
电子
透射
Hypoxia-ischemia, brain
Hyperbaric oxygenation
Synaptophysin
Microscopy, electron, transmission
