Se@SiO(2) nanocomposites suppress microglia-mediated reactive oxygen species during spinal cord injury in rats

Selenium (Se) is an essential trace element with strong antioxidant activity, showing a great prospect in the treatment of spinal cord injury (SCI). However, the narrow gap between the beneficial and toxic effects has limited its further clinical application. In this experiment, we used porous Se@SiO(2) nanocomposites (Se@SiO(2)) modified by nanotechnology as a new means of release control to investigate the anti-oxidative effect in SCI. In vitro Se@SiO(2) toxicity, anti-oxidative and anti-inflammatory effects on microglia were assayed. In vivo we investigated the protective effect of Se@SiO(2) to SCI rats. Neurological function was evaluated by Basso, Beattie and Bresnahan (BBB). The histopathological analysis, microglia activation, oxidative stress, inflammatory factors (TNF-α, IL-1β and IL-6) and apoptosis were detected at 3 and 14 days after SCI. The favorable biocompatibility of Se@SiO(2) suppressed microglia activation, which is known to be associated with oxidative stress and inflammation in vivo and in vitro. In addition, Se@SiO(2) improved the rat neurological function and reduced apoptosis via caspase-3, Bax and Bcl-2 pathways in SCI. Se@SiO(2) was able to treat SCI and reduce oxidative stress, inflammation and apoptosis induced by microglia activation, which may provide a novel and safe strategy for clinical application.