Fig. 4.

CE alleviated MI/R injury by regulating LTCC in vivo and vitro. After treatment of CE (7.5, 15, 30 mg/kg) and nisoldipine (2 mg/kg) or Bay-K-8644 (30 μg·kg⁻¹) for three days, the rats were subjected to IR surgery. (a) Experimental protocol 2 to detect the effects of CE on MI/R injury in rat. (b) The myocardial infarction area was detected by Evans Blue/TTC staining, and quantification of infarct size (IS/AAR) and ischemic size (AAR/LV) was also displayed (n = 5 per group). (c) Representative trace of M−mode echocardiography performed 48 h after MI/R injury in a rat study and quantitative analysis of left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) using echocardiography (n = 5 per group). (d) The levels of LDH, AST, CK-MB, and Troponin-I were detected (n = 5 per group). (e) The fluorescence images of ROS and calcium levels (scale bar, 200 μm) in hiPSC-CMs were displayed after the treatment of nisoldipine (100 nM) or Bay-K-8644 (8 nM) (n = 6 per group). (f) The fluorescence intensity of ROS (left) and intracellular calcium (right) was statistically represented in the histogram. (g) After the intervention of nisoldipine (100 nM) or Bay-K-8644 (8 nM) for 2 h, NRVMs were incubated using CE (8 μM) for 12 h and then cell viability was detected after HR injury (n = 16 per group). The data were expressed as the mean ± SD. ^###P < 0. 001 vs sham (control) group; *P < 0.05 vs IR (HR) group, ^**P < 0.01 vs IR (HR) group, ^***P < 0.001 vs IR (HR) group; ^&&&P < 0.001 vs IR + CE (HR + CE) group.