Literature DB >> 18787991

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

Wei Yan1, Han-Dong Wang, Lin Zhu, Xiao-Mei Feng, Liang Qiao, Wei Jin, Ke Tang.   

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.

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Year:  2008        PMID: 18787991     DOI: 10.1080/02699050802372174

Source DB:  PubMed          Journal:  Brain Inj        ISSN: 0269-9052            Impact factor:   2.311


  4 in total

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  4 in total

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