Magnesium silicate nanosheets enable sustained hydrogen release to attenuate secondary brain injury following intracerebral hemorrhage.

Abstract

Intracerebral hemorrhage (ICH) causes severe secondary brain injury through oxidative stress, neuroinflammation, and apoptosis. This study synthesized pH-responsive magnesium silicate nanosheets (MGNs) capable of sustained hydrogen release, especially under acidic conditions. In a collagenase-induced ICH mouse model, oral MGN administration produced dose-dependent improvements in neurological function, reductions in brain edema and hematoma volume, preservation of neuronal integrity, suppression of pro-inflammatory cytokines, and decreased apoptotic signaling. MGNs outperformed conventional 3% hydrogen gas inhalation in neuroprotective efficacy and demonstrated a favorable biosafety profile across systematic evaluation. These findings position MGNs as a promising nanoplatform for sustained hydrogen delivery in the context of hemorrhagic brain injury.

Mechanism

MGNs release hydrogen continuously under acidic conditions, suppressing neuronal apoptotic pathways and reducing pro-inflammatory cytokine production, thereby mitigating secondary brain injury following ICH.