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. 2019 May 7;10:496. doi: 10.3389/fphar.2019.00496

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Copyright © 2019 Qin, Zhang, Yang, Li, Xu, Yao, Zhang, Gonzalez and Yao.

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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UGT1A9 catalyzes the glucuronidation of fraxetin. (A) Kinetic profiles for fraxetin-8-O-glucuronide (G1) and fraxetin-7-O-glucuronide (G2; 0.5–80 μM) generated by UGT1A9. (B) kinetic profiles for G1 and G2 (0.5–80 μM) generated by the HeLa1A9 cell lysate; in each panel, the inset shows the corresponding Eadie–Hofstee plot. (C) Inhibitory effects of magnolol (1 μM), niflumic acid (10 μM), and androsterone (10 μM) on the glucuronidation (formation of G1 and G2) at 4 μM of fraxetin. (D) Inhibitory effects of magnolol (1 μM), niflumic acid (10 μM), and androsterone (10 μM) on fraxetin-O-glucuronidation (formation of G1 and G2) at 20 μM. Data are expressed as mean ± SD. ^∗∗,^##p < 0.01, or ^∗∗∗,^###p < 0.001 as compared with the control.