Role of Keap1/Nrf2 system in host defense against acute lung injury.

在本研究中，我们研究了Nrf 2在预防急性肺损伤发展中的作用。缺乏Nrf 2的小鼠易受几种刺激诱导的急性肺损伤，如博来霉素、脂多糖和流感病毒。在Nrf 2缺陷小鼠的肺中，几种自卫基因的诱导低于野生型小鼠。核因子-κB的活化和促炎细胞因子的诱导在Nrf 2缺陷型小鼠中显著高于野生型小鼠。结果表明，Nrf 2是一个关键因素，在保护免受发展的急性肺损伤诱导的环境刺激。

In the present study, we investigated the role of Nrf2 in protection against the development of acute lung injury. Mice lacking Nrf2 were susceptible to acute lung injury induced by several stimuli, such as bleomycin, lipopolysaccaride, and influenza virus. The induction of several self-defense genes was lower in the lungs of Nrf2-deficient mice than in wild-type mice. Activation of nuclear factor-κB and induction of proinflammatory cytokines were significantly higher in Nrf2-deficient mice than in wild-type mice. Results indicate Nrf2 is a pivotal factor in protection against the development of acute lung injury induced by environmental stimuli.