Journal of Capital Medical University ›› 2017, Vol. 38 ›› Issue (1): 42-46.doi: 10.3969/j.issn.1006-7795.2017.01.009

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Normobaric hyperoxia protect cerebral ischemia/reperfusion injured rats by downregulating voltage-dependent anion channel protein

Shi Wenjuan, Qi Zhifeng, Liu Kejian   

  1. Xuanwu Hospital, Capital Medical University, Beijing Geriatric Medical Research Center, Cerebrovascular Diseases Research Institute, Beijing 100053, China
  • Received:2016-11-28 Online:2017-01-21 Published:2017-01-20
  • Supported by:
    This study was supported by National Natural Science Foundation of China (81620108011,81571175), Beijing Nova Program (Z141107001814045).

Abstract: Objective To observe the effect of normobaric hyperoxia (NBO) on expression of voltage-dependent anion channel (VDAC), cytochrome C (CytC) and cleaved caspase-3 induced by cerebral ischemia-reperfusion injury in rats, and preliminarily explore the mechanism of NBO treatment on prevention of apoptosis. Methods Fifteen healthy adult male Sprague-Dawley (SD) rats (280-320 g) were divided randomly into three groups:Sham group (n=3), Normoxia group (n=6) and NBO group (n=6). A model operation of MCAO was performed using intraluminal suture method. The rats underwent MCAO for 1.5 h plus 24 h reperfusion. After model operation the rats of sham group and normoxia group breathed normal air, and instead NBO group rats breathed 100% oxygen until reperfusion. Western blotting was used to test the expression of VDAC, CytC and cleaved caspase-3 protein in ischemic penumbra region. Results Western blotting results showed that compared with the sham group, the VDAC protein expression of ischemic penumbra was increased (P<0.05) in the normoxia group, and compared with the normoxia group, the expression of VDAC protein in ischemic penumbra region was statistically significantly reduced (P<0.05) in NBO group. Compared with the normoxia group, the expressions of CytC protein and cleaved caspase-3 protein in ischemic penumbra region were statistically significantly decreased (P<0.05) in NBO group. Conclusion NBO treatment may inhibit cerebral ischemia-induced apoptosis by downregulating the excessive expression of voltage-dependent anion channel protein in ischemic penumbra region, thus to play a protective role in the ischemia/reperfusion injured brain.

Key words: cerebral ischemia-reperfusion, normobaric hyperoxia(NBO), voltage-dependent anion channel(VDAC), apoptosis

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