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中国临床药理学与治疗学 ›› 2012, Vol. 17 ›› Issue (9): 967-971.

• 基础研究 • 上一篇    下一篇

环氧化酶2过表达对铝盐致大鼠海马神经元损伤的影响

吴柯, 谢灵瑶, 杨俊卿   

  1. 重庆医科大学药学院,重庆市生物化学与分子药理学重点实验室,重庆 400016
  • 收稿日期:2011-12-30 修回日期:2012-04-06 发布日期:2012-09-25
  • 通讯作者: 杨俊卿,通信作者,男,教授,博士生导师,研究方向:神经、精神药理。Tel: 13637809247 E-mail: cqjqyang2004@yahoo.com.cn
  • 作者简介:吴柯,男,讲师,研究方向:神经药理。Tel: 13330200467 E-mail: wuke1997@yahoo.com.cn
  • 基金资助:
    国家自然科学基金资助(30672211)

Effects of COX-2 overexpression on hippocampal neuronal damage induced by aluminum in rat

WU Ke, XIE Ling-Yao, YANG Jun-qin   

  1. Department of Pharmacology, Chongqing Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing Medical University, Chongqing 400016, China
  • Received:2011-12-30 Revised:2012-04-06 Published:2012-09-25

摘要: 目的 研究环氧化酶2(COX-2)过表达与铝盐致大鼠海马神经元损伤间的关系。方法 原代海马神经元培养 7 d,予以铝盐负荷(终浓度 200 μmol/L)建立大鼠海马神经元损伤模型,以神经元转染COX-2过表达腺病毒(MOI=100),Western Blot检测COX-2的蛋白表达水平,酶化学法检测海马神经元超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、乳酸脱氢酶(LDH)漏出率及MTT值,倒置荧光显微镜观察海马神经元病理形态变化。结果 COX-2过表达腺病毒转染的神经元COX-2蛋白表达增加(P<0.01),SOD活性、MDA含量、LDH漏出率、MTT值,以及大鼠海马神经元细胞的形态和结构未见明显异常变化。而COX-2过表达腺病毒转染在铝盐负荷基础上的海马神经元细胞MTT值和SOD活性明显下降,LDH漏出率和MDA含量明显上升(P<0.01或P<0.05),表现为严重的细胞损伤。结论 单纯的一定程度COX-2过表达不会造成神经元明显损伤,但可增加神经元对铝盐损伤的敏感性。

关键词: COX-2过表达, 铝盐, 神经元损伤

Abstract: AIM: To study the relationship between COX-2 overexpression and hippocampal neuronal damage induced by aluminum. METHODS: Neonatal SD rats less than 24 h were used to establish the model of primary cultured hippocampal neuron treated aluminum overload(200 μmol/L). The primary cultured hippocampal neurons were transfected by adenovirus over expressing COX-2.The expression of COX-2 protein in hippocampal neurons was measured by Western Blot. The SOD and LDH activities and MDA contents were detected respectively. The cell viability was measured by MTT.The fluorescence detection was used to observe the change of neuronal pathomorphology. RESULTS: The transfection of adenovirus overexpressing COX-2 significantly increased the expression of COX-2 protein(P<0.01),without effects on neuronal pathomorphology, cell viability, the SOD activity and MDA content. However, it remarkably increased damage to neurons induced by aluminum overload.CONCLUSION: Acertain degree of COX-2 overexpression may not cause serious injury of neurons, but can increase the damage susceptibility of neurons undergoing aluminum overload.

Key words: COX-2 overexpression, Aluminum, Neuronal damage

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