Bach1 gene ablation reduces steatohepatitis in mouse MCD diet model

  • Inoue Motoki
    Department of Medicine and Molecular Science, Graduate School of Biomedical Sciences, Hiroshima University
  • Tazuma Susumu
    Department of General Internal Medicine, Hiroshima University Hospital
  • Kanno Keishi
    Department of General Internal Medicine, Hiroshima University Hospital
  • Hyogo Hideyuki
    Department of Medicine and Molecular Science, Graduate School of Biomedical Sciences, Hiroshima University
  • Igarashi Kazuhiko
    Department of Biochemistry, Tohoku University School of Medicine
  • Chayama Kazuaki
    Department of Medicine and Molecular Science, Graduate School of Biomedical Sciences, Hiroshima University

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説明

Bach1 is a transcriptional repressor of heme oxygenase-1 (HO-1, a.k.a. HSP-32), which is an inducible enzyme and has anti-oxidation/anti-inflammatory properties shown in various models of organ injuries. Since oxidative stress plays a pivotal role in the pathogenesis of nonalcoholic steatohepatitis (NASH), HO-1 induction would be expected to prevent the development of NASH. In this study, we investigated the influence of Bach1 ablation in mice on the progression of NASH in methionine-choline deficient (MCD) diet model. Bach1 ablation resulted in significant induction of HO-1 mRNA and its activity in the liver. When fed MCD diet, Bach1−/− mice exhibited negligible hepatic steatosis compared to pronounced steatohepatitis in wild type mice with 6-fold increase in hepatic triglyceride content. Whereas feeding of MCD diet decreased mRNA expressions of peroxisome proliferator-activated receptor (PPAR) α and microsomal triglyceride transfer protein (MTP) in wild type mice, there were no change in Bach1−/− mice. In addition, hepatic concentration of malondialdehyde (MDA), a biomarker for oxidative stress as well as plasma alanine aminotransferase (ALT) was significantly lower in Bach1−/− mice. These findings suggest that Bach1 ablation exerts hepatoprotective effect against steatohepatitis presumably via HO-1 induction and may be a potential therapeutic target.<br>

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詳細情報 詳細情報について

  • CRID
    1390282679649336320
  • NII論文ID
    130004466637
  • DOI
    10.3164/jcbn.09-122gfr
  • ISSN
    18805086
    09120009
  • PubMed
    21373270
  • 本文言語コード
    en
  • データソース種別
    • JaLC
    • Crossref
    • CiNii Articles
    • OpenAIRE
  • 抄録ライセンスフラグ
    使用不可

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