低氧预适应对缺氧缺血性脑损伤大鼠脑保护作用及机制研究  

Study on the protective effect and mechanism of hypoxic preconditioning on the brain in rats after hypoxic-ischemic brain damage

作　　者：李敦臣[1] 刘钢[1] 姜荣燕[1] 李希红[1] 杨琳[1] 殷宪敏[1] 

机构地区：[1]泰山医学院附属医院儿科,泰安271000

出　　处：《中国新生儿科杂志》2010年第3期157-160,共4页Chinese Journal of Neonatology

基　　金：山东省教育厅科研发展计划项目(J08LG71);山东省卫生厅医药卫生科技发展计划项目(2009HZ096)

摘　　要：目的探讨低氧预适应对缺氧缺血性脑损伤(HIBD)大鼠脑保护作用及相关机制。方法选用生后7dSD大鼠48只,随机分为对照组(6只)、假手术组(6只)、HIBD组(18只)和HIBD+低氧预适应(HPC)组(18只)。用湿化的氧浓度为8%的氮氧混合气体以0.3L/min的流量灌入建立HPC模型。用免疫荧光和激光共聚焦显微镜技术,分别行大脑皮层和海马神经细胞凋亡、Bcl-2和Caspase-3表达强度的检测。结果HIBD、HIBD+HPC组TUNEL染色阳性细胞较假手术组明显增多(P<0.05);HIBD+HPC组较HIBD组明显减少(P<0.05)。对照组和假手术组大脑皮层、海马可见极少量Bcl-2和Caspase-3表达,两组比较差异无统计学意义(P>0.05);HIBD、HIBD+HPC组Bcl-2和Caspase-3表达明显高于假手术组,HIBD+HPC组Bcl-2表达高于HIBD组,Caspase-3表达低于HIBD组(P均<0.05)。结论低氧预适应过程中,HIBD大鼠大脑皮层和海马区通过Bcl-2的高表达和Caspase-3的低表达,抵御神经细胞凋亡,参与脑保护机制。Objective To explore the protective effect and mechanism of hypoxic preconditioning on the brain in SD rats after hypoxic-ischemic brain damage（HIBD）. Methods Fortyeight seven-day-old SD rats were used and divided into 4 groups randomly ： control group, sham operation group, HIBD group and HIBD ＋ hypoxic preconditioning group （HPC）. HPC model was established by exposure a humidified gas mixture of 8% oxygen/92% nitrogen at an approximate flow rate of 0.3 L/ min. With the research methods and techniques of immunofluorescence and confoeal laser scanning, microscope measurement of cell apoptosis, fluorescence intensity of Bcl-2 and Caspase-3 in cortex and hippocampus was done respectively. Results More TUNEL stained positive cells could be found in HIBD group and HIBD ＋ HPC group than those in sham operation group （ P 〈 0.05 ）. TUNEL stained positive cells decreased rapidly in HIBD ＋ HPC group than those in HIBD group （P 〈 0. 05 ）. Fluorescence intensity of Bcl-2 and Caspase-3 was faint in control group and sham operation group, and there was no difference between them （P 〉 0. 05）. The expression of Bcl-2 and Caspase-3 in both HIBD group and HIBD ＋ HPC group was higher than that in sham operation group. The expression of Bcl-2 in HIBD ＋ HPC group was even higher than that in HIBD group, whereas the expression of Caspase-3 in HIBD ＋ HPC was significantly lower than that in HIBD （ P 〈 0. 05 ）. Conclusion Apoptosis of cortex and hippocampus cells in SD rats after HIBD is resisted via increased expression of Bcl-2 and lowered activity of Caspase-3 in the cortex and hippocampus, and brain cells are thereby protected during hypoxic preconditioning.

关 键 词：缺氧缺血 脑 低氧预适应 凋亡 Bcl-2 CASPASE-3 大鼠 

分 类 号：R363[医药卫生—病理学]