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. 2019 Feb 1;10:48. doi: 10.3389/fphar.2019.00048

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Copyright © 2019 Xiang, Yang, Liu, He, Zhang, Li, Zhang and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic diagram of potential mechanisms that CBS improves liver injury and hepatic bile acid accumulation in estrogen-induced cholestasis. In liver and intestine, CBS activates protein expression and nuclear translocation of FXR, and then alters the expression of downstream genes. Regarding transporters, CBS decreases NTCP levels to reduce hepatic bile acid (BA) uptake and increases BSEP, MRP2, MRP3, and MRP4 levels to augment BA efflux. Moreover, CBS reduces BA biosynthesis in the liver by repressing BA synthetic enzymes, CYP7A1 and CYP8B1, via hepatic FXR-SHP and intestinal FXR-FGF15 axes. Lastly, CBS increases BA metabolism by increasing the expression of CYP3A2, CYP2B10, and SULT2A1.