Fig. 5

Compound C counteracts the cardioprotective effects of geniposide in mice. A–C Quantification of myocardium tissue (LDH, CK, CK-MB) on plasma of MI/RI mice treated with Compound C or GEN (n = 6). D SOD2 enzymatic activity of mice as indicated group assayed with a commercial kit (n = 5). E Quantitative assessment of analysis of LV ejection fraction (LVEF), fractional shortening (LVFS), left ventricular end-diastole diameter (LVEDd), and LV end-systolic diameter (LVESd) (n = 6). F Representative TTC–Evans Blue stained sections of hearts and quantitative data of the LV infarct size. Infarct size (%) was expressed as the percentage of infarct area relative to the total left ventricular area. the nonischemic section shown in blue area, red represent risk area, and the infarct region is stained white (n = 6). G Detection of ROS in myocardium by DHE staining. Compared with sham, the DHE fluorescence intensity in the myocardium of the vehicle-treated infarcted group was sharply increased and Compound C ablated the protective effect of geniposide (n = 6). H Immunofluorescence TUNEL staining after Compound C or GEN treatment (n = 6). The data for each group were shown as the mean ± SD; ^#p < 0.05, ^##p < 0.01 vs. Sham group; *p < 0.05, **p < 0.01 vs. I/R + Vehicle group