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

Brain Inj. 2008 Sep;22(10):802-10. doi: 10.1080/02699050802372174.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / etiology
  • Acute Lung Injury / metabolism*
  • Animals
  • Antioxidants / metabolism*
  • Brain Injuries / complications
  • Brain Injuries / metabolism*
  • Gene Expression Regulation / physiology
  • Heme Oxygenase-1 / metabolism*
  • Immunohistochemistry
  • Macrophages, Alveolar / metabolism
  • Male
  • NADP / metabolism
  • NF-E2-Related Factor 2 / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Reverse Transcriptase Polymerase Chain Reaction
  • Signal Transduction / physiology
  • Trachea / metabolism

Substances

  • Antioxidants
  • NF-E2-Related Factor 2
  • NADP
  • Heme Oxygenase-1