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A Selenium Nanocomposite Protects the Mouse Brain from Oxidative Injury Following Intracerebral Hemorrhage

Authors Yang Y, Deng G, Wang P, Lv G, Mao R, Sun Y, Wang B, Liu X, Bian L, Zhou D

Received 26 November 2020

Accepted for publication 7 January 2021

Published 4 February 2021 Volume 2021:16 Pages 775—788

DOI https://doi.org/10.2147/IJN.S293681

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yan Shen


Yong Yang,1,* Guoying Deng,2,* Peng Wang,1 Guangzhao Lv,1 Rui Mao,1 Yuhao Sun,3 Baofeng Wang,3 Xijian Liu,4 Liuguan Bian,3 Dong Zhou1

1Department of Neurosurgery, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, People’s Republic of China; 2Trauma Center, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 201620, People’s Republic of China; 3Department of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 200025, People’s Republic of China; 4College of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, Shanghai, 201620, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Liuguan Bian
Department of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, 197 Rui Jin Er Road, Shanghai, 200025, People’s Republic of China
Tel +86 21 64370045 Ext 666091
Fax +86 21 64333548
Email blg11118@rjh.com.cn
Dong Zhou
Department of Neurosurgery, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, No. 106 Zhongshan Er Road, Yuexiu District, Guangzhou, 510080, People’s Republic of China
Tel +86 20 83827812 Ext 61521
Email zhoudong5413@163.com

Background: Intracerebral hemorrhage (ICH) is a common neurological crisis leading to high mortality and morbidity. Oxidative stress-induced secondary injury plays a critical role in neurological deterioration. Previously, we synthesized a porous Se@SiO2 nanocomposite and identified their therapeutic role in osteonecrosis of the femoral head. Whether this nanocomposite is neuroprotective remains to be elucidated.
Methods: A porous Se@SiO2 nanocomposite was synthesized, and its biosafety was determined using a CCK-8 assay. The neuroprotective effect was evaluated by TUNEL staining, and intracellular ROS were detected with a DCFH-DA probe in SH-SY5Y cells exposed to hemin. Furthermore, the effect of the nanocomposite on cell apoptosis, brain edema and blood–brain barrier permeability were evaluated in a collagenase-induced ICH mouse model. The potential mechanism was also explored.
Results: The results demonstrated that Se@SiO2 treatment significantly improved neurological function, increased glutathione peroxidase activity and downregulated malonaldehyde levels. The proportion of apoptotic cells, brain edema and blood–brain barrier permeability were reduced significantly in ICH mice treated with Se@SiO2 compared to vehicle-treated mice. In vitro, Se@SiO2 protected SH-SY5Y cells from hemin-induced apoptosis by preventing intracellular reactive oxygen species accumulation.
Conclusion: These results suggested that the porous Se@SiO2 nanocomposite exerted neuroprotection by suppressing oxidative stress. Se@SiO2 may be a potential candidate for the clinical treatment of ICH and oxidative stress-related brain injuries.

Keywords: selenium nanocomposites, oxidative stress, blood–brain barrier, brain edema, apoptosis

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