[1]袁野,杨俊卿,周岐新.脑缺血再灌注致小鼠神经元退行性变进程中自由基水平和SOD-1表达的变化[J].第三军医大学学报,2011,33(12):1211-1215.
 Yuan Ye,Yang Junqing,Zhou Qixin.Level of free radicals and expression of SOD-1 in neuronal degeneration mice due to cerebral ischemia-reperfusion[J].J Third Mil Med Univ,2011,33(12):1211-1215.
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脑缺血再灌注致小鼠神经元退行性变进程中自由基水平和SOD-1表达的变化(/HTML )
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
33卷
期数:
2011年第12期
页码:
1211-1215
栏目:
论著
出版日期:
2011-06-30

文章信息/Info

Title:
Level of free radicals and expression of SOD-1 in neuronal degeneration mice due to cerebral ischemia-reperfusion
作者:
袁野杨俊卿周岐新
重庆医科大学药学院药理学教研室
Author(s):
Yuan Ye Yang Junqing Zhou Qixin
Department of Pharmacology,College of Pharmacy,Chongqing Medical University, Chongqing, 400016, China
关键词:
再灌注损伤神经变性疾病超氧化物歧化酶自由基小鼠
Keywords:
reperfusion injury neuronal degeneration superoxide dismutase free radical mice
分类号:
R743.31;R741.02
文献标志码:
A
摘要:
目的    探讨脑缺血再灌注(ischemia/reperfusion,I/R)致神经元退行性变自由基和SOD-1表达的时程变化。    方法    NIH小鼠160只,分为I/R组和假手术组,每组80只。抽取并回输约40%总血量加双侧颈总动脉夹闭20 min建立I/R损伤模型。分别于术后5、15、30、60 d以光学显微镜观察神经元损伤;Morris水迷宫评价学习记忆能力;分光光度计法检测SOD-1活性和丙二醛(MDA)含量;RT-PCR和Western blot分别检测海马SOD-1 mRNA和蛋白表达。    结果    假手术组脑组织MDA含量、SOD-1活性及蛋白、mRNA表达分别为(0.549±0.049) nmol/mg、(55.134±4.076) U/mg、30.413±2.962和104.541±18.825。与假手术组比较,I/R组小鼠学习记忆能力显著降低,术后5、15、30、60 d脑组织MDA含量[(0.673±0.087)、(0.782±0.101)、(0.719±0.094)、(1.084±0.140) nmol/mg]进行性显著升高(P<0.05);术后5 d和15 d I/R组SOD-1活性[(42.522±3.701)、(37.011±4.843) U/mg]和蛋白表达(23.145±3.476、15.746±2.344)显著降低(P<0.05);术后30 d和60 d I/R组SOD-1活性[(51.801±6.706)、(50.202±6.488) U/mg]与假手术组间差异无显著性(P>0.05),但SOD-1蛋白表达(40.587±6.154、44.263±6.597)较假手术组显著升高(P<0.05);各组SOD-1 mRNA表达水平无显著差异(P>0.05);组织学检测显示I/R组海马出现进行性神经元核固缩加重和神经元丢失。    结论    I/R致小鼠神经元退行性变与SOD-1表达和功能异常和氧化应激进行性增强有关。
Abstract:
Objective    To study the changes of three radicals and expression of SOD-1 in neuronal degeneration due to cerebral ischemia/reperfusion(I/R) in mice.     Methods    One hundred and sixty NIH mice were divided into I/R group and sham operation group, 80 mice in each group. A cerebral I/R model was established by drawing out and reperfusing 40% of the whole blood volume and clamping the bilateral carotid arteries for 20 min. On days 5, 15, 30, and 60 after cerebral I/R, neuronal injury was observed under a light microscope, learning and memory ability of the mice was assessed with Morris water maze, hippocampal SOD-1 activity and malonaldehyde (MDA) level were measured with a spectrophotometer and expressions of SOD-1 mRNA and protein in the hippocampus were detected by RT-PCR and Western blotting, respectively.     Results    The MDA level, SOD-1 activity, expression level of SOD-1 protein and mRNA in sham operation group were 0.549±0.049 nmol/mg, 55.134±4.076 U/mg, 30.413±2.962 and 104.541±18.825, respectively. The learning and memory ability of mice was significantly lower in I/R group than in sham operation group. The MDA level in brain tissue of I/R group was significantly higher on days 5, 15, 30, and 60 days after I/R (0.673±0.087, 0.782±0.101, 0.719±0.094, and 1.084±0.140 nmol/mg) than sham operation group (P<0.05). The activity of SOD-1 (42.522±3.701 and 37.011±4.843 U/mg) and the expression level of SOD-1 protein (23.145±3.476 and 15.746±2.344) were significantly lower than sham operation group after I/R on days 5 and 15 (P<0.05). No significant difference was observed in SOD-1 activity after I/R 30 and 60 d between the two groups (51.801±6.706 vs 50.202±6.488 U/mg, P>0.05),while the expression of SOD-1 protein was significantly higher in I/R group than in sham operation group (44.263±6.597 vs 40.587±6.154, P<0.05). However, no significant difference was found in expression level of SOD-1 mRNA (P>0.05). Histology showed the progressive loss and karyopyknosis of neurons in hippocampi of I/R group.     Conclusion    Neuronal degeneration due to cerebral I/R is related with the progressively increased oxidative stress and abnormal SOD-1 expression and activity.

参考文献/References:

袁野, 杨俊卿, 周岐新. 脑缺血再灌注致小鼠神经元退行性变进程中自由基水平和SOD-1表达的变化[J].第三军医大学学报,2011,33(12):1211-1215.

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更新日期/Last Update: 2011-05-24