摘要
目的探讨脑缺血预处理对新生Wistar鼠脑CA1区突触素和热休克蛋白70（HSP70）变化的影响.方法通过阻断7日龄新生Wistar大鼠右侧颈总动脉制备脑缺血模型,设置假手术组、缺血再灌注组、预缺血-缺血再灌注组.用免疫组化法检测三组新生鼠不同时点海马CA1区脑组织神经细胞突触素和HSP70的动态变化,并光镜下观察脑组织病理改变.结果突触素：缺血再灌注组和预缺血-缺血再灌注组海马CA1区突触素表达在再灌注后第3天开始增加,分别为10.76±0.99、15.89±0.59,7 d时达高峰,分别为13.14±0.76、18.33±1.11,14 d时分别为12.01±0.71、15.13±1.10,仍高于假手术组（8.31±0.01）,三组比较差异均有统计学意义（P＜0.05）;HSP70假手术组海马CA1区有极少量HSP70表达.缺血再灌注组和预缺血-缺血再灌注组海马CA1区HSP70表达在再灌注后6 h开始增高,分别为1.48±0.82、1.90±0.10,24 h达高峰,分别为8.15±0.99、11.32±0.96,3 d时开始下降,分别为3.42±0.21、5.31±0.51,三组比较差异均有统计学意义（P＜0.05）.预缺血组海马CA1区病理改变较缺血再灌注组轻.结论脑缺血预处理对再次脑缺血所致脑神经细胞损伤有保护作用;新生鼠脑缺血后3～14 d海马CA1区神经细胞突触素表达增加可反映受损神经细胞突触再生,说明受损神经细胞具有代偿再生重塑功能;脑缺血6 h后HSP70表达增多可能与神经细胞内源性保护机制有关.
Objective To investigate the expressions of synaptophysin and heat shock protein 70（HSP 70）in hippocampal CA1 region after cerebral ischernic preconditioning in 7-day-old Wistar rats. Methods Cerebral ischernia model was made by occluding right carotid artery in 7-day-old Wistar rats. The Wistar rats were randomly divided into preischemia-reperfusion group, ischerma-reperfusion group and sham-operation group. The pathologic changes in the brain were observed by microscope, and immunohistochernistry method was used to measure the expressions of synaptophysin, heat shock protein70（HSP70） in the hippocampal CA1 region at different times of reperfusion. Results The expression of synaptophysin in hippocampal CA1 region in cerebral ischemia-reperfusion group and ischemia-reperfusion group was increased at the 3rd day after reperfusion（10. 76＋-0. 99, 15. 89＋-0. 59, respectively）, reached the highest level at day 7（13. 14＋-0. 76, 18. 33＋-1. 11, respectively）, and remained at a high level at day 14（12. 01＋-0. 71, 15. 13＋-1. 10, respectively） ; all were higher than that of the control （8. 31 ＋-0. 05, P〈0. 05）. The corrected optical density（COD）value of preisehermiareperfusion group was significantly higher than that of the ischemiaeperfusion group. Few expressions of HSP70 in hippocampal CA1 region was found in Sham-operation group. The expression of HSP70 in hippocampal CA1 region in ischemia-reperfusion group and preischemia-reperfusion group was increased at 6 h after reperfusion（1.48＋-0. 82, 1.90＋-0. 10, respectively）, reached the highest level at 24 h（8. 15＋-0. 99, 11.32＋- 0. 96, respectively）, then decreased at day 3 （3. 42＋-0. 21, 5. 31＋-0. 51, respectively） ; the COD value of ischemia-reperfusion group was significantly higher than that of the ischemia-reperfusion group. The damages in the preischemia-reperfusion group were less severe than that of the ischemia-reperfusion group. Conclusions Cerebral ischemic preconditioning has protective effect on brain neuron cell damage caused by re-ischemia. Synaptophysin is a better index to investigate the regeneration of neuron and nervous axons and its increased expression demonstrate the neuroplasticity of regeneration of the central nervous system. The expression of HSP70 in early stage may also play a role in the protective effects of brain after ischemia.
出处
《中华围产医学杂志》
CAS
2006年第4期266-269,I0007,共5页
Chinese Journal of Perinatal Medicine
基金
贵州省卫生厅资助(D-174)
