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BioMed Research International
Volume 2016 (2016), Article ID 8263926, 9 pages
Research Article

SIRT3 Expression Decreases with Reactive Oxygen Species Generation in Rat Cortical Neurons during Early Brain Injury Induced by Experimental Subarachnoid Hemorrhage

1Department of Neurosurgery, The 175th Hospital of PLA, Affiliated Southeast Hospital of Xiamen University, Center of Traumatic Neurosurgery in Nanjing Military Command, 269 Middle Zhanghua Road, Zhangzhou 363000, China
2Department of Neurosurgery, Changzheng Hospital, Second Affiliated Hospital of Second Military Medical University, 415 Feng Yang Road, Shanghai 200003, China

Received 23 May 2016; Revised 16 August 2016; Accepted 23 August 2016

Academic Editor: Robert M. Starke

Copyright © 2016 Wei Huang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Sirtuin3 (SIRT3) is an important protein deacetylase which predominantly presents in mitochondria and exhibits broad bioactivities including regulating energy metabolism and counteracting inflammatory effect. Since inflammatory cascade was proved to be critical for pathological damage following subarachnoid hemorrhage (SAH), we investigated the overall expression and cell-specific distribution of SIRT3 in the cerebral cortex of Sprague-Dawley rats with experimental SAH induced by internal carotid perforation. Results suggested that SIRT3 was expressed abundantly in neurons and endothelia but rarely in gliocytes in normal cerebral cortex. After experimental SAH, mRNA and protein expressions of SIRT3 decreased significantly as early as 8 hours and dropped to the minimum value at 24 h after SAH. By contrast, SOD2 expression increased slowly as early as 12 hours after experimental SAH, rose up sharply at the following 12 hours, and then was maintained at a higher level. In conclusion, attenuated SIRT3 expression in cortical neurons was associated closely with enhanced reactive oxygen species generation and cellular apoptosis, implying that SIRT3 might play an important neuroprotective role during early brain injury following SAH.