Ultrastructural mitochondria changes in perihematomal brain and neuroprotective effects of Huperzine A after acute intracerebral hemorrhage
Authors Lu H, Jiang M, Lu L, Zheng G, Dong Q
Received 10 July 2015
Accepted for publication 20 August 2015
Published 13 October 2015 Volume 2015:11 Pages 2649—2657
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Wai Kwong Tang
Haiying Lu,1,* Mei Jiang,2,* Lei Lu,3 Guo Zheng,1 Qiang Dong3
1Department of Neurology, Nanjing Children’s Hospital, Nanjing Medical University, Nanjing, 2Department of Neurology, Shanghai Pudong New Area Gongli Hospital, Shanghai, 3Department of Neurology, Huashan Hospital, Fudan University, Shanghai, People’s Republic of China
*These authors contributed equally to this work
Aim: The purpose of the study was to observe the ultrastructural changes of neuronal mitochondria in perihematomal brain tissue and assess the therapeutic potential of Huperzine A (HA, a mitochondrial protector) following intracerebral hemorrhage (ICH).
Methods: Brain hemorrhage was induced in adult Sprague Dawley rats by injecting autologous blood into the striatum and then removing the brains 3, 6, 12, 24, or 48 hours later to analyze mitochondrial ultrastructure in a blinded manner. Parallel groups of ICH rats were treated with HA or saline immediately after ICH. Perihematomal apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), caspase-3 activation and cytochrome C translocation were tracked by immunoblots, and neurobehavioral test results were compared between the groups.
Results: Mitochondria in perihematomal neurons demonstrated dramatic changes including mitochondrial swelling, intracristal dilation, and decreased matrix density. HA treatment decreased mitochondrial injury and apoptosis, inhibited caspase-3 activation and cytochrome C translocation, and improved behavioral recovery.
Conclusion: These data show that ICH induces dramatic mitochondrial damage, and HA exhibits protective effects possibly through ameliorating mitochondrial injury and apoptosis. Collectively, these findings suggest a new direction for novel therapeutics.
Keywords: apoptosis, intracerebral hemorrhage, mitochondria, huperzine A, neuroprotection
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