Ferroptosis involved in sevoflurane-aggravated young rats brain injury induced by liver transplantation

Liver transplantation is the only treatment available for pediatrics with end-stage liver disease. However, neurological damage is prone to occur after liver transplantation, especially in children. Accumulating evidence has shown that sevoflurane is closely linked to brain injury induced by liver transplantation. However, the study on the role of sevoflurane in brain injury induced by liver transplantation is rare and needs to be further investigated. The study is aiming to investigate the effects of sevoflurane on brain injury induced by liver transplantation and its underlying mechanisms. The brain injury rat model was built through 70% hepatic ischemia-reperfusion (HIR) of young rats. We detected the ferroptosis and brain injury after HIR by histological, transmission electron microscope analyses, western blot, and Enzyme-linked immunosorbent assays. And we detected the level of ferroptosis in brain by using sevoflurane during HIR compared with HIR without using sevoflurane. At the same time, we use iron inhibitor deferoxamine (DFO) to verify that the brain injury was caused by ferrotosis of brain. The results indicated that the pathological injury, ferroptosis indicators, and brain injury indicators were aggravated in the sevoflurane group compared with the HIR group, the decrease in the degree of brain injury and ferroptosis was observed in the group using DFO. Collectively, the results suggest that ferroptosis may mediate sevoflurane-aggravated young rats' brain injury induced by liver transplantation. Our findings provide a potential therapeutic target for brain injury after pediatric liver transplantation.