Inhibition of ferroptosis protects sepsis-associated encephalopathy

Schematic diagram illustrating the possible mechanisms of Nrf2/HO-1 signaling pathway of ferroptosis in Sepsis-associated encephalopathy. Sepsis induced depletion of GSH, lipid peroxidation, and accumulation of iron, result in neuroinflammation and cognitive impairment in SAE mice, which suggested that ferroptosis play a role in the pathogenesis of SAE. However, Fer-1 relieved mitochondrial dysfunction, reduced oxidation stress and inhibited hippocampal ferroptosis by activating Nrf2/OH-1 signaling pathway, which improved cognitive function in SAE mice.