Research Article

Propofol Activation of the Nrf2 Pathway Is Associated with Amelioration of Acute Lung Injury in a Rat Liver Transplantation Model

Figure 6

A diagram of propofol-induced activation of Nrf2 under conditions of oxidative stress. Under normal conditions, a single Keap1 protein is able to target multiple Nrf2 proteins for destruction by the ubiquitin-proteasome system. Endogenously generated ROS alter the interaction between Nrf2 and its repressor under oxidative stress, resulting in the accumulation of Nrf2 in the cytoplasm and Nrf2 translocates to the nucleus. As an antioxidant, propofol enhances the effect of the endogenous activator of Nrf2 pathway. Propofol accelerates the dissociation of Nrf2 from Keap1 which leads to more Nrf2 translocation to the nucleus under conditions of oxidative stress. Through binding with Maf and ARE, Nrf2 regulates the expression of its downstream target genes (HO-1, NQO1, γ-GCS, etc.) to prevent oxidative stress and damage.
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