Traumatic brain injury induces the activation of the Nrf2-ARE pathway in the lung in rats

Abstract

Background: Acute lung injury (ALI) is a frequent but poorly understood complication of traumatic brain injury (TBI). The Nrf2-ARE pathway has been proved to be essential for protection against diffuse inflammation and oxidative damage, which are both involved in ALI following TBI. However, whether the Nrf2-ARE pathway is activated after TBI in the lung hasn’t been studied.

Methods and procedures: In the present study, the nuclear Nrf2 protein level was detected by Western blot and the mRNA levels of heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase-1 (NQO1), two Nrf2-regulated gene products, were determined by RT-PCR at 24 hours after TBI. In addition, the expression of Nrf2 and HO-1 was localized by immunohistochemical study.

Main outcomes and results: After TBI, the nuclear Nrf2 protein level in the lung was significantly increased and the mRNA levels of both HO-1 and NQO1 were also up-regulated. Moreover, immunohistochemical study showed that both Nrf2 and HO-1 were mainly localized in tracheobronchial epithelium and alveolar macrophages.

Conclusion: These results suggest that the Nrf2-ARE pathway is activated in the lung after TBI.

• Acute lung injury
• heme oxygenase-1
• NF-E2-related factor 2
• Quinone oxidoreductase-1
• traumatic brain injury