摘要
目的:探讨脑震荡损伤对大鼠海马区代谢物水平的影响及其病理机制.方法:将25只成年雄性SD大鼠随机分为对照组(n=10)和PCS组(n=15),采用Marmarou改良法复制大鼠脑震荡损伤模型,对脑震荡24h大鼠及对照组大鼠进行1H-MRS扫描后处死,对脑组织进行免疫组织化学和免疫荧光染色观察海马CA1区的残存锥体细胞和凋亡细胞的数量.结果:1H-MRS扫描结果显示,PCS组大鼠左侧海马区NAA/Cr水平(0.824±0.17)明显低于正常对照组(1.299±0.12),P<0.01;PCS组大鼠右侧海马NAA/Cr水平(0.792±0.17)明显低于正常对照组(1.287±0.18),P<0.01.PCS组大鼠海马CA1区小血管扩张淤血,锥体细胞呈代偿肥大与凋亡并存状态.免疫组织化学结果显示,PCS组大鼠海马CA1区NeuN阳性细胞数量(176.17±26.92)较正常对照组(228.33±26.34)明显减少,P<0.05;免疫荧光实验结果显示,PCS组海马CA1区凋亡细胞的数量(48.03±5.46)较正常对照组(35.49±7.75)明显增多,P<0.01.结论:脑震荡后大鼠双侧海马区神经细胞的代谢物水平均下降,海马CA1区残存锥体细胞数量减少和凋亡细胞增多,后者可能是代谢物水平变化的病理基础.
Objective： To explore the impairment effects of postconcussion syndrome on hip- pocampal metabolites level and its pathological mechanism. Methods： 25 male SD rats were randomly divided into control （n = 10） and PCS （n = 15） group, PCS animal model was set up by Marmarou＇s improvement means, nomal rear for 24 h, in vivo proton magnetic resonance spectroscopy （1H-MRS） was performed to detected hippocampal metabolites level, immunohistochemistry and immunofluorescence were employed to observe pyramidal cells remained and apoptosis cells in hippocampal CA1 region. Results： 1H-MRS scan found left hippocampal NAA/Cr level of PCS rats （0.824 ± 0.17） was lower than control （1.299 ± 0.12）, P 〈 0.01. In the right hippocampus, NAA/ Cr level of PCS rats （0.792 ± 0.17） was also lower than control rats （1.287 ± 0.18）, P 〈 0.01. Small vessel expansion, array rarefaction of pyramidal cell, cell hyperplasia and apoptosis were coexist in hippocampal CA1 region of PCS rats. Results from immunohistochemistry indicated NeuN positive cell in hippocampal CA1 region of PCS rats （176.17 ± 26.92） was significant less than control rats （228.33 ± 26.34）, P 〈 0.05. Immunofluorescence showed that apoptosis cells of PCS rats （48.03 ± 5.46） in CA1 region was more than control rats （35.49 ± 7.75）, P 〈 0.01. Conclusion： After postconcussion syndrome, metabolites levels of bilateral hippocampus decrease, pyramidal cells decrease and apoptosis cells increase in hippocampal CA 1 region. The latter may be the pathological foundations ofmetabolites levels alteration.
出处
《江汉大学学报（自然科学版）》
2010年第1期74-78,共5页
Journal of Jianghan University：Natural Science Edition
基金
湖北省教育厅科研计划重点项目(鄂教科[2007]4号)
湖北省卫生厅科研基金项目(鄂卫函[2007]54号)
