首页> 美国卫生研究院文献>Cellular and Molecular Gastroenterology and Hepatology >Cholangiopathy and Biliary Fibrosis in Cyp2c70-Deficient Mice Are Fully Reversed by Ursodeoxycholic Acid
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Cholangiopathy and Biliary Fibrosis in Cyp2c70-Deficient Mice Are Fully Reversed by Ursodeoxycholic Acid

机译:Cyp2C70缺陷小鼠的胆管病和胆汁纤维化通过熊胆酸完全逆转

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摘要

Bile acids (BAs) aid intestinal fat absorption and exert systemic actions by receptor-mediated signaling. BA receptors have been identified as drug targets for liver diseases. Yet, differences in BA metabolism between humans and mice hamper translation of pre-clinical outcomes. Cyp2c70-ablation in mice prevents synthesis of mouse/rat-specific muricholic acids (MCAs), but potential (patho)physiological consequences of their absence are unknown. We therefore assessed age- and gender-dependent effects of Cyp2c70-deficiency in mice.
机译:胆汁酸(BAS)辅助肠脂肪吸收并通过受体介导的信号传导施加全身作用。 BA受体已被鉴定为肝病的药物靶标。然而,人类与小鼠之间的BA代谢的差异阻碍了临床前后的翻译。 CYP2C70-FIES-FERSATION可防止合成小鼠/大鼠特异性杂体酸(MCAS),但其缺席的潜在(PATO)生理后果是未知的。因此,我们评估了CYP2C70缺乏小鼠的年龄和性别依赖性影响。

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