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. 2017 Mar 30;8:162. doi: 10.3389/fphar.2017.00162

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Copyright © 2017 Festa, De Marino, Carino, Sepe, Marchianò, Cipriani, Di Leva, Limongelli, Monti, Capolupo, Distrutti, Fiorucci and Zampella.

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) or licensor 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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In vitro screening on the library. (A) FXR transactivation on HepG2 cells. HepG2 cells were transfected with pSG5-FXR, pSG5-RXR, PGL4.70-Renilla, and p(hsp27) TKLUC vectors. Cells were stimulated with compounds 1–16 (1 and 10 μM). 6-ECDCA (6E, 1 and 10 μM) was used as positive control. (B) GPBAR1 transactivation on HepG2 cells. HepG2 cells were co-transfected with GPBAR1 and a reporter gene containing a cAMP responsive element in front of the luciferase gene. Cells were stimulated with 6-ECDCA (6E, 1 μM) and compounds 1–16 (1 and 10 μM). TLCA (10 μM) was used as positive control. Luciferase activity served as a measure of the rise in intracellular cAMP following activation of GPBAR1. In both panels, results are expressed as mean ± standard error. ^∗p < 0.05 versus not treated cells (NT).