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において四塩化炭素誘発性の肝線維症が緩和される

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

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<p>Background: Cirrhosis is a condition come from excessive liver fibrosis and followed by serious second diseases. 1.3 million people are died of cirrhosis in a year but there is no effective therapeutic medicine. α7 nicotinic acetylcholine receptor (α7nAChR), initially found a receptor related to neurotransmission, expresses on immune cells and activation of this receptor leads anti-inflammatory effect. However, there is few reports showing the relationship between α7nAChR and fibrosis.</p><p>Aim: Using α7nAChR knocked out mice (α7 KO), we investigated whether α7nAChR has any effect on liver fibrosis.</p><p>Methods: Liver fibrosis model mice were established with carbon tetrachloride (CCl4, 1 ml/kg, twice a week). The amount of collagen and pro-fibrotic mRNA expressions in livers were measured at 1.5 and 4 weeks.</p><p>Results: α7 KO treated with CCl4 showed significant decrease in liver fibrosis at 4 weeks compared to wild type mice (WT). Furthermore, mRNA expressions of Acta2, TGF-β1 and Col1a1 in α7 KO were significantly lower than WT at 1.5 weeks.</p><p>Conclusion: Increase of pro-fibrotic mRNA expression and liver fibrosis induced by CCl4 were alleviated in α7nAChR KO mice. These data suggested that α7nAChR might be a therapeutic target for cirrhosis.</p>

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