Fig. 8
Plasma AA concentration and cardiac function in patients with diabetic myocardial infarction and the molecular mechanism of AA cardioprotective effect. Serum cTnI and plasma AA & 6-keto-PGF1α concentrations of diabetic and non-diabetic patients were detected 2−4 h after MI onset, and echocardiography was performed 4−5 h after MI onset. A The serum cTnI concentration of MI and DM + MI patients. B Plasma concentration of AA. C Plasma concentration of 6-keto-PGF1α. D Representative images of echography. E Measurement of the ejection fraction. The ejection fraction of subjects with DM + MI decreased significantly. F Correlation analysis between FBG and AA. G Correlation analysis between blood cTnI and AA. H Schematic diagram of cardioprotection of AA in diabetic MI injury. **P < 0.01 and ***P < 0.001. Statistical analysis was carried out by a one-way ANOVA analysis. DM, diabetes mellitus; MI, acute myocardial infarction; HG: high glucose; OGD: oxygen deprivation; mtDNA:gDNA: mitochondrial DNA/genomic DNA; FBG: fasting blood glucose; cTnI, cardiac troponin I