中国组织工程研究

中国组织工程研究 ›› 2011, Vol. 15 ›› Issue (50): 9389-9392.doi: 10.3969/j.issn.1673-8225.2011.50.020

• 组织构建实验造模 experimental modeling in tissue construction • 上一篇    下一篇

局灶脑缺血再灌注成年模型大鼠大脑髓鞘相关蛋白的基因表达

李华杰1，吴  坚1，朱林凤1，包仕尧2   

  1. 1苏州大学附属第三医院神经内科(常州市第一人民医院），江苏省常州市  213003
    2苏州大学附属第二医院神经内科，江苏省苏州市 215004
  • 收稿日期:2011-06-18 修回日期:2011-08-27 出版日期:2011-12-10 发布日期:2011-12-10
  • 通讯作者: 李华杰☆，男，1972年生，山东省曹县人，汉族，2004年苏州大学毕业，博士，副主任医师，主要从事脑血管病基础和临床研究。 lihuajie0589@yahoo.com.cn
  • 作者简介:李华杰☆，男，1972年生，山东省曹县人，汉族，2004年苏州大学毕业，博士，副主任医师，主要从事脑血管病基础和临床研究。 lihuajie0589@yahoo.com.cn
  • 基金资助:

    常州市社会发展项目资助(cs2005206)，课题名称：“不同年龄、不同程度脑缺血后少突胶质细胞及其前体细胞反应特征的对比研究”。

Gene expression of myelin associated protein in adult rats after focal cerebral ischemia and reperfusion

Li Hua-jie1, Wu Jian1, Zhu Lin-feng1, Bao Shi-yao2   

  1. 1Department of Neurology, Third Affiliated Hospital of Soochow University (First People’s Hospital of Changzhou), Changzhou  213003, Jiangsu Province, China
    2Department of Neurology, Second Affiliated Hospital of Soochow University, Suzhou  215004, Jiangsu Province, China
  • Received:2011-06-18 Revised:2011-08-27 Online:2011-12-10 Published:2011-12-10
  • Contact: Li Hua-jie, Department of Neurology, Third Affiliated Hospital of Soochow University (First People’s Hospital of Changzhou), Changzhou 213003, Jiangsu Province, China lihuajie0589@yahoo.com.cn
  • About author:Li Hua-jie☆, Doctor, Associate chief physician, Department of Neurology, Third Affiliated Hospital of Soochow University (First People’s Hospital of Changzhou), Changzhou 213003, Jiangsu Province, China lihuajie0589@yahoo.com.cn
  • Supported by:

    the Changzhou Foundation for Social Development, No. cs2005206*

PDF

364

被引次数

2

摘要：

背景：髓鞘蛋白是少突胶质细胞的主要成分，研究脑缺血再灌注后大脑髓鞘相关蛋白基因表达的变化有助于探讨少突胶质前体细胞在缺血性脑损伤和修复中的作用。
目的：观察脑缺血再灌注后成年模型大鼠大脑髓鞘蛋白相关基因，在脑缺血后不同时间及部位表达变化和差异。
方法：以线栓法制作成年SD大鼠局灶性脑缺血再灌注模型，采用5′末端标记地高辛的寡核苷酸探针荧光原位核酸分子杂交检测模型大鼠再灌注后早期大脑梗死中心区、梗死周边区和梗死对侧区皮质髓鞘蛋白脂质蛋白mRNA、髓鞘碱性蛋白mRNA和髓鞘转录因子1 mRNA表达变化。
结果与结论：在梗死中心区，脑缺血再灌注后早期3种髓鞘相关蛋白基因表达均明显减少；在梗死周边区，再灌注后1 d时3种髓鞘相关蛋白基因表达与对照组比较无明显变化，之后逐渐增加，至14 d时均高于对照组(P  < 0.05，0.01)，以髓鞘转录因子1 mRNA阳性细胞数升高最早(7 d)最为显著(P < 0.01)。因此，成年SD大鼠脑缺血再灌注后急性期梗死周边区皮质髓鞘相关蛋白的基因表达增加，提示少突胶质前体细胞对脑缺血性损伤敏感，其可能参与了脑缺血后损伤的修复过程。

关键词: 少突胶质前体细胞, 缺血, 再灌注, 髓鞘蛋白, 基因, 大鼠

Abstract:

BACKGROUND: Myelin proteins are the main components in oligodendroglia cells. Research on gene expression changes of myelin related proteins after focal cerebral ischemia and reperfusion will help to understand the role of oligodendroglia cells in focal cerebral ischemia and reperfusion.
OBJECTIVE: To explore the gene expression change of myelin related proteins in different cerebral regions and at different time points after focal cerebral ischemia and reperfusion in adult model rats.
METHODS: Focal cerebral ischemia and reperfusion model in adult SD rats was constructed using suture method. The early phase mRNA expression changes of myelin proteolipid protein, myelin basic protein and myelin transcription factor 1 in the cerebral cortex regions of infraction center, infarction borders and contralateral area of infarction were detected by fluorescent in situ hybridization with the dig-labeled oligonucleotides.
RESULTS AND CONCLUSION: The gene expression of the three myelin related proteins in infraction center decreased significantly in the early phase of focal cerebral ischemia and reperfusion. In infarction borders, there was no significant change in the gene expression of the three myelin related proteins between experiment group and control group on the 1st day after focal cerebral ischemia and reperfusion. Then the gene expression of experiment group increased, and exceeded that of the control group on the 14th day after focal cerebral ischemia and reperfusion (P < 0.05, 0.01); the content of myelin transcription factor 1 positive cells raised the earliest (P < 0.01). The gene expression of cerebral cortex myelin related proteins in infarction borders increased after focal cerebral ischemia and reperfusion in adult SD rats. It indicates that oligodendrocyte precursors are sensitive to cerebral ischemic injury and may involve in the repairing process of cerebral post-ischemic injury.

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