Fig. 4.

Valsartan inhibited CK2 and protected KCNJ2/Kir2.1. a qPCR and immunoblots depicting the effect of valsartan on both CK2 and Kir2.1 in infarcted border and noninfarcted LVFW in MI rats. Both the upregulation of CK2 and the downregulation of Kir2.1 following MI were reversed by valsartan. *P < 0.05 vs. control; ^† P < 0.05 vs. MI; n = 10/group. b qPCR and immunoblots depicting the effect on CK2 in H9c2 cells. The upregulation of CK2 by hypoxia induced by CoCl₂ was depressed by valsartan. *P < 0.05 vs. control; ^† P < 0.05 vs. CoCl₂; n = 10/group. c qPCR and immunoblots depicting the effect on Kir2.1. The downregulation of Kir2.1 by hypoxia was improved by valsartan. Additionally, the over-expression of CK2 in the cells treated with valsartan abrogated this effect. *P < 0.05 vs. control; ^† P < 0.05 vs. CoCl₂; ^# P < 0.05 vs. CoCl₂ + valsartan; n = 10/group. d Autoradiograms and the EMSA quantification of Sp1 DNA-binding activity in rat hearts. The data are the fold values of DNA-binding activity in the MI+valsartan group compared with the MI group. *P < 0.05 vs. control; ^† P < 0.05 vs. CK2; n = 10/group. Values are means ± SDs