Figure 6From: Diabetic cardiomyopathy is associated with defective myocellular copper regulation and both defects are rectified by divalent copper chelationExpression and activity analyses of CCS and SOD1 in LV tissues from control, diabetic, and TETA-treated diabetic rats. A: RT-qPCR analysis of Ccs mRNA levels. Data are means ± SEM and presented relative to the respective controls which were set at 1: **P < 0.01, vs. control; ##P < 0.01 vs. diabetic: n = 9/group. B: Quantitative analysis of immunofluorescent signal area for CCS. Results are expressed as means of the percentages of corresponding cross-sectional areas. At least 40 sectional images/group were analyzed: **P < 0.01 vs. control; ##P < 0.01 vs. diabetic. C: Measurement of SOD1 activity by monitoring xanthine oxidase activity, which is inhibited by SOD1. The IC50 (50% inhibition activity of SOD) was detected by a colorimetric method at 450 nm and the results calculated as units/mg of total protein (based on a unit of SOD activity as the amount necessary to inhibit xanthine oxidation by 50%): **P < 0.01 vs. control; ##P < 0.01 vs. diabetic: n = 9/group. D: Measurement of protein levels of SOD1 in LV extracts by ELISA. Results were calculated as ng/mg total protein and are presented as the means of relative concentrations related to the control group, which was set at 1: **P < 0.01 control: n = 9/group.Back to article page