Intravenous Anesthetic Protects Hepatocyte from Reactive Oxygen Species-Induced Cellular Apoptosis during Liver Transplantation In Vivo

Figure 7

Propofol postconditioning reduces liver injury and the possible mechanisms. Under hepatic I/R condition, NADPH oxidase and TLR4/NF-κB pathway are activated. Endogenously, ROS were generated due to NADPH oxidase activation, resulting in the caspase-3-related apoptosis pathway as well as NF-κB pathway activation. Amount of proinflammatory cytokines was produced after NF-κB p65 pathway activation. Propofol postconditioning inhibited Nox2 (gp91^phox and p47^phox) which could lead to downregulation of ROS generation and finally reduced hepatic I/R injury.