書誌事項
- タイトル別名
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- Carbon tetrachloride mediated liver fibrosis is alleviated in α7 nicotinic acetylcholine receptor knockout mice
抄録
<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>
収録刊行物
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- 日本薬理学会年会要旨集
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日本薬理学会年会要旨集 93 (0), 1-P-058-, 2020
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390002184883038208
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- NII論文ID
- 130007811248
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- ISSN
- 24354953
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可