Neural Regeneration Research ›› 2013, Vol. 8 ›› Issue (1): 76-82.doi: 10.3969/j.issn.1673-5374.2013.01.010

Previous Articles     Next Articles

Changes in secretory pathway Ca2+ -ATPase 2 following focal cerebral ischemia/reperfusion injury

Tonglin Lu, Zhiping Hu, Liuwang Zeng, Zheng Jiang   

  1. Department of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China
  • Received:2012-08-16 Revised:2012-11-18 Online:2013-01-05 Published:2013-01-05
  • Contact: Zhiping Hu, Doctoral supervisor, Professor, Department of Neurology, Second Xiangya Hospital, Central South University, Changsha 410011, Hunan Province, China,huzhiping2007@yahoo.com.cn.
  • About author:Tonglin Lu☆, Studying for doctorate.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81171239, Frontier Research Project of Central South University in China, No. 2177-721500065, and the Graduate Degree Thesis Innovation Foundation of Central South University in China.

Abstract:

This study aimed to investigate changes in secretory pathway Ca2+ -ATPase 2 expression following cerebral ischemia/reperfusion injury, and to define the role of Ca2+ -ATPases in oxidative stress. A rat model of cerebral ischemia/reperfusion injury was established using the unilateral middle cerebral artery occlusion method. Immunohistochemistry and reverse transcription-PCR assay results showed that compared with the control group, the expression of secretory pathway Ca2+ -ATPase 2 protein and mRNA in the cerebral cortex and hippocampus of male rats did not significantly change during the ischemic period. However, secretory pathway Ca2+ -ATPase 2 protein and mRNA expression reduced gradually at 1, 3, and 24 hours during the reperfusion period. Our experimental findings indicate that levels of secretory pathway Ca2+ -ATPase 2 protein and mRNA expression in brain tissue change in response to cerebral ischemia/reperfusion injury.

Key words: neural regeneration, brain injury, cerebral infarction, secretory pathway Ca2+ -ATPase 2, Golgi apparatus,   Ca2+ oscillations, manganese, focal cerebral ischemia, oxidative damage,  Ca2+ -ATPase, grants-supported paper, photographs-containing paper, neuroregeneration