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

Figure 4.

Figure 4

Phanginin A increased PDE4 activity and inhibited the cAMP pathway by activating SIK1. (A–D) Primary mouse hepatocytes were pretreated with 0.5 μM of pan-SIK inhibitor HG-9-91-01 for 30 min and cotreated with 5 or 10 μM of phanginin A and then the PDE4 activity (A), cAMP concentration (B), PKA activity (C), and CREB phosphorylation (D) were detected. ∗P < 0.05 and ∗∗P < 0.01 vs controls under basal conditions. #P < 0.05 and ##P < 0.01 vs controls under HG-9-91-01 conditions. (E–J) Primary mouse hepatocytes were pretreated with SIK1 siRNA for 48 h and then treated with 5 μM or 10 μM of phanginin A and then the PDE4 activity (E), cAMP concentration (F), and PKA activity (G) were examined. Primary mouse hepatocytes were treated with 5 μM of phanginin A after SIK1 interference and then the CREB phosphorylation (H), mRNA expression of G6P (I), and PEPCK (J) were evaluated. ∗P < 0.05 and ∗∗P < 0.01 vs controls under negative control conditions. ##P < 0.01 vs controls under siSIK1 conditions. All of the results are presented as the mean ± SEM (n = 5).