Remimazolam alleviates intracerebral hemorrhage outcomes by suppressing neuronal ferroptosis.

Abstract

Intracerebral hemorrhage (ICH) is a severe stroke subtype associated with high morbidity and mortality. Secondary brain injury after ICH involves complex pathological mechanisms, including neuronal apoptosis, neuroinflammation, and oxidative stress, yet effective therapeutic interventions remain limited. Remimazolam, an ultra-short-acting sedative anesthetic, has emerged as a promising candidate due to its reported neuroprotective and anti-inflammatory effects. However, its precise role in ICH pathogenesis remains unclear. Using a murine ICH model, we found that remimazolam treatment significantly improved neurological function, reduced cerebral edema, and attenuated neuronal apoptosis. Given the critical role of ferroptosis in ICH-induced brain injury, we further investigated its involvement. Mechanistic investigations revealed that remimazolam significantly reduced the accumulation of ROS and Fein both perihematomal regions of ICH mice and HT22 cells treated with hemin. These findings highlight remimazolam's potential to inhibit ferroptosis and improve cognitive function in ICH, offering a promising therapeutic strategy for ICH.