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

Affiliation

Yang Y(#)(1), Deng G(#)(2), Wang P(1), Lv G(1), Mao R(1), Sun Y(3), Wang B(3), Liu X(4), Bian L(3), Zhou D(1).
Author information:
(1)Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, People's Republic of China.
(2)Trauma Center, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 201620, People's Republic of China.
(3)Department of Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, 200025, People's Republic of China.
(4)College of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, Shanghai, 201620, People's Republic of China.
(#)Contributed equally

Abstract

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.