基础医学与临床 ›› 2011, Vol. 31 ›› Issue (11): 1229-1233.

• 研究论文 • 上一篇    下一篇

脑缺血/再灌注致神经元退行性变进程中自由基水平和SOD2表达相关

袁野1,杨俊卿2,2,周岐新2,3   

  1. 1. 重庆医科大学药学院药理学教研室
    2.
    3. 重庆医科大学
  • 收稿日期:2010-11-17 修回日期:2011-01-27 出版日期:2011-11-05 发布日期:2011-11-02
  • 通讯作者: 袁野 E-mail:yuanyecq@yahoo.com.cn
  • 基金资助:
    国家重点基础研究发展计划

Relationship Between SOD2 Expression and Free Radical Level in Neurodegeneration Induced by Ischemia-reperfusion

  • Received:2010-11-17 Revised:2011-01-27 Online:2011-11-05 Published:2011-11-02

摘要: 目的 探讨脑缺血/再灌注(I/R)致神经元退行性变所涉及的自由基和SOD2表达的时程变化及其相互关系。方法 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。组织学检测神经元损伤;Morris水迷宫检测学习记忆能力;分光光度计法检测SOD2活性和丙二醛(MDA)含量;Western blot检测SOD2蛋白表达。结果 与假手术组相比,I/R组小鼠学习记忆能力显著降低,海马MDA含量进行性显著升高(P<0.05);I/R术后5、15、30和60 d组海马SOD2活性(14.69+2.49 U/mg.pro,14.15+2.41 U/mg.pro,15.07+2.67 U/mg.pro,15.55+2.64 U/mg.pro)和蛋白表达(9.20+1.23,5.40+1.03,4.90+0.92,5.60+0.59)均显著低于假手术组(P<0.05);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SOD2蛋白表达和活性保持低水平状态而氧化应激进行性增强有关。

关键词: 缺血/再灌注, 神经元退行性变, 超氧化物歧化酶-2, 自由基

Abstract: Objective To investigate the changes of time process of SOD2 and free radicals in neurodegeneration induced by cerebral ischemia-reperfusion(I/R). Methods Cerebral I/R model was established through drawing out and reperfusing 40% of the whole blood volume in combination with clamping the carotid arteries for 20 min. Histological observation was performed to evaluate the neural damage; learning and memory ability was detected by Morris water maze; SOD2 activity and malonaldehyde(MDA) were determined by spectrophotometer; and expression of SOD2 was detected by western blot. Results Compared with sham group, the learning and memory ability of I/R group was significantly decreased, the hippocampal MDA level of I/R group was clearly increased in a time-dependent manner (P<0.05). SOD2 activity (14.69+2.49 U/mg.pro, 14.15+2.41 U/mg.pro, 15.07+2.67 U/mg.pro, 15.55+2.64 U/mg.pro)and protein expression (9.20+1.23, 5.40+1.03, 4.90+0.92, 5.60+0.59) of 5th d, 15th d, 30th d, and 60th d I/R group were lower than sham group (P<0.05). Histological test indicated there existed the loss and karyopyknosis of neurons in hippocampi of I/R group. Conclusion I/R-induced neurodegeneration may be related to the steady decreases of SOD2 expression and activity and increase of oxidative stress.

Key words: Ischemia-reperfusion, Neurodegeneration, Superoxide dismutase-2, Free radical

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