As shown in Figure 4, the expression levels of Keap1 were lower in rats that received OALT (Groups M, LP, HP, and NAC, P < 0.05 versus Group S).
As shown in Figure 5, the levels of HO-1 and NQO1 were significantly higher in rats that received OALT (Groups M, LP, HP, and NAC, P < 0.05, versus Group S), especially in rats pretreated with propofol (Groups LP and HP, P < 0.05, versus Group M).
The main findings of the present experiments were that propofol reduced the decline in oxygenation, pulmonary edema (as assessed by increase in the W/D ratio), reactive oxygen species ([H.sub.2][O.sub.2]) and lipid peroxidation (MDA), and histologic alteration induced by OALT through the Nrf2 antioxidant response pathway.
Specifically, we have previously shown that inflammation during OALT increased alveolocapillary permeability in the lung 35], and Nrf2 played an important role in antioxidative stress during OALT .
However, the levels of Nrf2, HO-1, and NQO1 apparently were insufficient to prevent lung oxidative damage induced by OALT, as serious lung injury still occur.