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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Taurine and Niacin Block Lung Injury and Fibrosis by Down-Regulating Bleomycin-Induced Activation of Transcription Nuclear Factor-κB in Mice ,

Gopalakrishnan Gurujeyalakshmi, Yingjin Wang and Shri N. Giri
Journal of Pharmacology and Experimental Therapeutics April 2000, 293 (1) 82-90;
Gopalakrishnan Gurujeyalakshmi
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Yingjin Wang
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Shri N. Giri
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Abstract

The effects of taurine (T) and niacin (N) on bleomycin (BL)-induced increased production of tumor necrosis factor-α (TNF-α), interleukin (IL)-1α, IL-6, and transforming growth factor-β (TGF-β) levels in the bronchoalveolar lavage fluid (BALF), and increased collagen content and nuclear factor-κB (NF-κB) activation in the lungs were investigated in mice. The mice were intratracheally instilled with saline (SA) or BL (0.1 U/mouse/50 μl) under ketamine and xylazine anesthesia. They had ad libitum access to diet containing 2.5% niacin (w/w) or the same control diet (CD) and water with and without taurine (1%) 3 days before intratracheal instillation and throughout the study. The mice were sacrificed at different times for collecting BALF and lungs, which were appropriately processed for various measurements. Treatment with taurine and niacin attenuated the BL-induced increases in proinflammatory cytokines such as IL-1α, TNF-α, IL-6, and TGF-β in BALF and lung hydroxyproline content of the mice in BL + TN groups. Reverse transcription-polymerase chain reaction analysis of total RNA from whole lung was performed to assess the induction of TNF-α and IL-1 mRNAs as markers of NF-κB activation. The NF-κB DNA-binding activity in whole-lung extract was evaluated by electrophoretic mobility shift assay. This revealed a progressive increase in NF-κB activation and IkBα depletion in lungs from mice in BL + CD groups from day 1 through day 21 compared with the corresponding SA + CD control groups. Treatment with taurine and niacin generally inhibited the BL-induced increases in the nuclear localization of NF-κB and preserved IκBα protein in BL + TN groups. This may be one of the mechanisms for the antifibrotic effect of taurine and niacin.

Footnotes

  • Send reprint requests to: Shri N. Giri, Ph.D., Department of Molecular Biosciences, School of Veterinary Medicine, University of California-Davis, Davis, CA 95616-8741. E-mail: sngiri{at}ucdavis.edu

  • ↵1 This research was supported by National Heart, Lung, and Blood Institute Grant R01-56262.

  • ↵2 A preliminary report of this work was presented in part at the International Taurine Symposium; Certosa di Pontignano, Siena, Italy, August 4–8, 1999.

  • Abbreviations:
    BL
    bleomycin
    IL
    interleukin
    TGF
    transforming growth factor
    TNF
    tumor necrosis factor
    MCP
    monocyte chemoattractant protein
    NF-κB
    nuclear factor-κB
    ROS
    reactive oxygen species
    T
    taurine
    N
    niacin
    SA
    saline
    CD
    control diet
    IT
    intratracheal
    BALF
    bronchoalveolar lavage fluid
    RT-PCR
    reverse transcription-polymerase chain reaction
    AP-2
    activator protein-2
    TBS-T
    Tris-buffered saline-Tween
    • Received July 1, 1999.
    • Accepted December 14, 1999.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 293 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 293, Issue 1
1 Apr 2000
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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Taurine and Niacin Block Lung Injury and Fibrosis by Down-Regulating Bleomycin-Induced Activation of Transcription Nuclear Factor-κB in Mice ,

Gopalakrishnan Gurujeyalakshmi, Yingjin Wang and Shri N. Giri
Journal of Pharmacology and Experimental Therapeutics April 1, 2000, 293 (1) 82-90;

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Research ArticleGASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Taurine and Niacin Block Lung Injury and Fibrosis by Down-Regulating Bleomycin-Induced Activation of Transcription Nuclear Factor-κB in Mice ,

Gopalakrishnan Gurujeyalakshmi, Yingjin Wang and Shri N. Giri
Journal of Pharmacology and Experimental Therapeutics April 1, 2000, 293 (1) 82-90;
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