Journal of Capital Medical University ›› 2015, Vol. 36 ›› Issue (5): 709-713.doi: 10.3969/j.issn.1006-7795.2015.05.009

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Effects of normobaric hyperoxia on activation of astrocyte following cerebral ischemia-reperfusion in rats

Shi Wenjuan, Liang Jia, Dong Wen, Qi Zhifeng, Liu Kejian   

  1. Cerebrovascular Diseases Research Institute, Xuanwu Hospital, Capital Medical University, Beijing Geriatric Medical Research Center, Beijing 100053, China
  • Received:2015-07-14 Online:2015-10-21 Published:2015-10-20
  • Contact: 刘克建 E-mail:kliu@salud.unm.edu
  • Supported by:
    This study was supported by National Natural Science Foundation of China (81171242, 81200928).

Abstract: Objective To observe the effect of normobaric hyperoxia (NBO) on GFAP (the activation marker of astrocyte) and connexin43 expression induced by cerebral ischemia-reperfusion injury in rats, and preliminarily explore the effect of NBO treatment on activation of astrocytes. Methods A total of 15 healthy adult male Sprague-Dawley (SD) rats (280-320 g) were randomly divided into Sham group (n=3), normoxia group (n=6) or NBO group (n=6). A model of middle cerebral artery occlusion for 1.5 h and reperfusion for 24 h was induced by using the intraluminal suture method. The sham group and the normoxia group rats breathed normal air, and instead NBO group rats were exposed to 100% oxygen after ischemia from 5 minutes until reperfusion. Immunofluorescence staining and Western blot were used to observe the expression of glial fibrillary acidic protein and connexin 43 in basal ganglia and cortex after cerebral ischemia.Results Immunofluorescence staining results showed that compared with the normoxia group, the number of GFAP positive cells in the ischemic cortex of NBO group was significantly reduced with the processes and fluorescence intensity decreased. Western blot results showed that compared with the normoxia group, the expression of GFAP protein was decreased in NBO group, and GFAP expression in the ischemic cortex of NBO group was statistically significantly reduced (P<0.05), and it was consistent with the immunofluorescence staining results. Compared with the sham group, the Cx43 protein expression was decreased in the normoxia group and that in the ischemic cortex of the normoxia group was statistically significantly reduced (P<0.01). Compared with the normoxia group, the Cx43 protein expression was increased in NBO group and that in the ischemic cortex of NBO group was statistically significantly increased (P<0.01). The Cx43 protein expression in basal ganglia did not change significantly. Conclusion NBO treatment decreased the excessive activation of astrocyte probably through increasing Cx43, therefore, NBO may play a protective role in the ischemia-reperfusion injured brain.

Key words: cerebral ischemia, normobaric hyperoxia, astrocyte, cortex, basal ganglia

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