Fig. 3

Oroxylin A alleviates microvascular obstruction and platelet activation to prevent MI progression. A, Masson’s trichrome staining of heart tissues from wild-type mice on day 7 post-MI. OroA (40 mg/kg once per day, o.g.) was administered for 7 days following MI surgery. The infarct size was quantified as a percentage of LV area (n = 8). Scale bar = 2 mm. B, Representative M-mode echocardiograms of the three study groups on day 7 post-MI. Echocardiography quantification of LVEF, LVFS, LVESV, LVEDV, LVDs and LVDd in mice of three study groups (n = 8). C, CD61 (platelet marker) staining of heart tissues from three study groups. Representative images are shown along with quantification of CD61-positive areas, expressed as a percentage of the field (n = 8). Scale bar = 50 μm (high magnification view) and 1 mm (low magnification view). D, OroA inhibited platelet activation after MI. On day 7 post-MI, washed platelets were separated, and activated by collagen (1 µg/mL) and thrombin (0.05 U/mL). Representative histograms obtained by flow cytometry show P-selectin (CD62P) exposure and activated integrin αIIbβ3 (JON/A) on the platelet surface (n = 8). The dotted lines highlight the mean values of the fluorescence intensities of P-selectin (CD62P) exposure and integrin αIIbβ3 (JON/A) activation on platelets from the vehicle-treated MI mice. Statistical analyses were performed using unpaired two-tailed Student’s t-test in (A), and one-way ANOVA followed by Tukey’s multiple comparison test in (B - D). NS, no significance; *P < 0.05; **P < 0.01; ***P < 0.001. MI, myocardial infarction; LV, left ventricular; LVEF, LV ejection fraction; LVFS, LV fractional shortening; LVESV, LV end-systolic volume; LVEDV, LV end-diastolic volume; LVDs, LV dimension-systole; LVDd, LV dimension-diastole