Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis
J. Clin. Invest. Rajesh K. Thimmulappa, et al. 116:984 doi:10.1172/JCI25790 [Go to this article.]

Figure 11
Pretreatment with exogenous antioxidants alleviates inflammation in Nrf2-deficient mice. (A) NF-κB–mediated luciferase reporter activity in Nrf2^–/– MEFs pretreated for 1 hour with NAC (10 mM) and/or GSH-monoethyl ester (GSH) (1 mM) after 3 hours of LPS (0.5 μg/ml) and/or TNF-α (10 ng/ml) stimulus. Data are presented as mean α SEM (n = 4). *Differs from vehicle control. ^†Differs from group that was treated with LPS or TNF-α only. P < 0.05. (B) Expression of TNF-α, IL-1β, and IL-6 by real-time PCR at 30 minutes in the lungs of Nrf2^–/– mice pretreated with NAC after LPS (i.p., 60 μg per mouse) challenge. (C) BAL fluid analysis at 6 hours in lungs of Nrf2^–/– mice pretreated with NAC after LPS (i.p., 60 μg per mouse) challenge. Nrf2^–/– mice were pretreated with 3 doses of NAC (500 mg/kg body weight, i.p., every 4 hours). Data are presented as mean α SEM. n = 4. ^#Differs from only LPS treatment. P < 0.05. (D) LPS-induced mortality in Nrf2^–/– and Nrf2^+/+mice pretreated with NAC. Age-matched male Nrf2^–/–(n = 10) and Nrf2^+/+ mice (n = 10) were pretreated with NAC (i.p., 500 mg/kg body weight) and/or saline every day for 4 days followed by LPS challenge (1.5 mg per mouse). Mortality was assessed every 12 hours for 5 days. **Mice pretreated with NAC had improved survival comped with vehicle-pretreated mice. P < 0.05.