Carbon tetrachloride mediated liver fibrosis is alleviated in α7 nicotinic acetylcholine receptor knockout mice

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  • Mihara Taiki
    Dept. of Vet. Pharmacol., Grad. Sch. Of Agri. & Life Sci., The Univ. of Tokyo
  • Kaji Noriyuki
    Dept. of Vet. Pharmacol., Azabu Univ.
  • Hori Masatoshi
    Dept. of Vet. Pharmacol., Grad. Sch. Of Agri. & Life Sci., The Univ. of Tokyo

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Other Title
  • 四塩化炭素誘発性肝線維化モデルはα7ニコチン様アセチルコリン受容体ノックアウトマウスで緩和される

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<p>Background: Cirrhosis is a condition come from excessive liver fibrosis and followed by serious secondary diseases, but there is no effective therapeutic medicine. α7 nicotinic acetylcholine receptor (α7nAChR), initially found as a receptor related to neurotransmission on neural cells. This receptor also expresses on immune cells to do anti-inflammatory action. However, there is few reports showing the relationship between α7nAChR and fibrosis.</p><p>Aim: We investigated whether α7nAChR has any effects on liver fibrosis and what is the mechanism.</p><p>Methods: Liver fibrosis model mice were established with CCl4. The pro-fibrotic mRNA expressions and collagen content in livers were measured at 1.5 and 4 weeks. Moreover, we performed immunohistochemical staining and RT-PCR to determine which cells were involved in the mechanism.</p><p>Results: α7nAChR KO mice treated with CCl4 showed significant decrease in pro-fibrotic mRNA expressions at 1.5 weeks and liver fibrosis at 4 weeks compared to WT mice. Furthermore, hepatocytes around fibrosis area expressed ACh transferase and activated hepatic stellate cells expressed α7nAChR.</p><p>Conclusion: The severity of fibrosis was significantly decreased in α7nAChR KO mice. Moreover, it is suggested that ACh produced by hepatocytes might stimulate hepatic stellate cells to promote collagen production.</p>

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