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Figure 6 | Cardiovascular Diabetology

Figure 6

From: Diabetic cardiomyopathy is associated with defective myocellular copper regulation and both defects are rectified by divalent copper chelation

Figure 6

Expression 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.

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