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Background: Pulmonary fibrosis is a progressive and lethal disorder. Although the precise mechanisms ofpulmonary fibrosis are not fully understood, oxidant/antioxidant and Th1/Th2 balances may play an important rolein many of the processes of inflammation and fibrosis. The transcription factor Nrf2 acts as a critical regulator forvarious inflammatory and immune responses by controlling oxidative stress. We therefore investigated theprotective role of Nrf2 against the development of pulmonary fibrosis.Methods: To generate pulmonary fibrosis, both wild-type C57BL/6 mice and Nrf2-deficient mice of the samebackground were administered bleomycin intratracheally.Results: The survival of Nrf2-deficient mice after bleomycin administration was significantly lower than that of wildtypemice. The degree of bleomycin-induced initial pulmonary inflammation and pulmonary fibrosis was muchmore severe in Nrf2-deficient mice than in wild-type mice. The expression of antioxidant enzymes and phase IIdetoxifying enzymes was significantly reduced in the lungs of Nrf2-deficient mice, concomitant with an elevationof lung 8-isoprostane level, compared with wild-type mice. The expression of Th2 cytokines, such as interleukin-4and interleukin-13, was significantly elevated in the lungs of Nrf2-deficient mice with an increase in the number ofTh2 cells that express GATA-binding protein 3.Conclusions: The results indicated that Nrf2 protects against the development of pulmonary fibrosis by regulatingthe cellular redox level and lung Th1/Th2 balance. Thus, Nrf2 might be an important genetic factor in thedetermination of susceptibility to pulmonary fibrosis.

収録刊行物

  • Respiratory research

    Respiratory research (11), 31, 2010-03

    BioMed Central

キーワード

各種コード

  • NII論文ID(NAID)
    120002104447
  • NII書誌ID(NCID)
    AA12051434
  • 本文言語コード
    ENG
  • 資料種別
    journal article
  • ISSN
    1465-9921
  • データ提供元
    IR 
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