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. 2020 Jun 26;41:101045. doi: 10.1016/j.molmet.2020.101045

Figure 3.

Figure 3

Phanginin A inhibited gluconeogenesis by increasing PDE4 activity in primary mouse hepatocytes. (A) Primary mouse hepatocytes were serum-starved for 4 h and the mRNA levels of PDE4 isoforms were detected (n = 5). (B) Primary mouse hepatocytes were treated with phanginin A for 3 h and then the PDE4 activity was detected (n = 5). (C) The direct effect of 10 μM of phanginin A on PDE4 enzymes (n = 5). (D–E) Primary mouse hepatocytes were pretreated with a PDE4 inhibitor (1 μM of roflumilast) for 30 min and cotreated with 5 or 10 μM of phanginin A and then the cAMP levels (n = 5) (D) and gluconeogenesis (n = 7) (E) were evaluated. (F) Primary mouse hepatocytes were pretreated with a PDE3 inhibitor (100 μM of cilomilast) for 30 min and cotreated with 5 or 10 μM of phanginin A and then gluconeogenesis was measured (n = 5). All of the results are presented as the mean ± SEM. ∗P < 0.05 and ∗∗P < 0.01 vs controls under basal conditions. ##P < 0.01 vs controls under roflumilast or cilomilast conditions.