Fig. 8.

Pae interacted with CK2α and restored the activity of CK2α in high glucose (HG)-treated cardiomyocytes. (a) Listing of potential candidates involved in kinase activity. (b-e) PKA inhibitor (PKAi) or CK2α inhibitor (TBB) was pre-administered to the cardiomyocytes in the HG + Pae group and then the expression of phosphorylated Stat3 (p-Stat3), total Stat3 and Opa1 were quantified. (f) The 2D and 3D structure of Pae. (g) Binding mode between Pae and CK2α. CK2α is represented with the cartoon, and the representative binding residues are indicated by lines. (h) Relative CK2α activity. (i) Representative blots and quantitative analysis of CK2α expression. (j) Interaction between CK2α and Jak2 or Stat3 determined by co-immunoprecipitation. NG, normal glucose (5.5 mmol/L); HG, high glucose (33 mmol/L); Pae, paeonol (100 μmol/L). n = 6 in each group. All data are shown as means ± SEM. *P < 0.05, **P < 0.01.