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

• Published in: International journal of nanomedicine 2021-01, Vol.16, p.775-788
• Main Authors: Yang, Yong, Deng, Guoying, Wang, Peng, Lv, Guangzhao, Mao, Rui, Sun, Yuhao, Wang, Baofeng, Liu, Xijian, Bian, Liuguan, Zhou, Dong
• Format: Article
• Language: English
• Subjects: Analysis; Animals; Antioxidants - pharmacology; Apoptosis; Apoptosis - drug effects; Biological activity; Biomarkers - metabolism; blood brain barrier; Blood-Brain Barrier - drug effects; Blood-Brain Barrier - pathology; Brain; Brain - drug effects; Brain - pathology; brain edema; Brain Edema - complications; Brain Edema - drug therapy; Cell Line, Tumor; Cerebral Hemorrhage - complications; Cerebral Hemorrhage - drug therapy; Cerebral Hemorrhage - pathology; Cytoprotection - drug effects; Disease Models, Animal; Edema; Flow cytometry; Hemin - toxicity; Humans; Injuries; Intracerebral hemorrhage; Laboratory animals; Male; Malondialdehyde - metabolism; Mice; Mice, Inbred C57BL; Nanocomposites; Nanocomposites - chemistry; Nanocomposites - toxicity; Nanocomposites - ultrastructure; Nanoparticles; Neuroblastoma; Neuroprotection - drug effects; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Original Research; Oxidative stress; Oxidative Stress - drug effects; Permeability; Reactive oxygen species; Reactive Oxygen Species - metabolism; Reactive Oxygen Species - pharmacology; Selenium; Selenium - pharmacology; Selenium - therapeutic use; selenium nanocomposites; Silicon Dioxide - pharmacology; Toxicity Tests
• ISSN: 1178-2013; 1176-9114; 1178-2013
• DOI: 10.2147/IJN.S293681

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@SiO nanocomposite and identified their therapeutic role in osteonecrosis of the femoral head. Whether this nanocomposite is neuroprotective remains to be elucidated. A porous Se@SiO 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. The results demonstrated that Se@SiO 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@SiO compared to vehicle-treated mice. In vitro, Se@SiO protected SH-SY5Y cells from hemin-induced apoptosis by preventing intracellular reactive oxygen species accumulation. These results suggested that the porous Se@SiO nanocomposite exerted neuroprotection by suppressing oxidative stress. Se@SiO may be a potential candidate for the clinical treatment of ICH and oxidative stress-related brain injuries.