Fig. 1.

BCI ameliorates cardiac injury in post-MI rats. (A) Experimental scheme showing the timing of (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) injections, myocardial infarction (MI) and echocardiography (ECHO) of rats. i.v., intravenous. (B) Representative M-mode tracings from ECHO of sham-operated and vehicle- or BCI-treated groups at 4 weeks post-MI. (C) The BCI treatment group showed improved ejection fraction and fractional shortening compared with the vehicle treatment group, and partially rescued heart function compared with the sham group (n=9–10). (D) BCI treatment improved left ventricle (LV) volumes and LV end-diastolic diameter (LVEDD) compared with vehicle treatment (n=9–10). (E) Masson's trichrome staining showing less fibrosis in BCI-treated hearts than in control hearts at 28 days post-MI (scale bar: 3 mm, n=9–10). (F) High-magnification images of Masson's trichrome and H&E staining showing decreased fibrosis in BCI-treated hearts at 28 days post-MI (scale bar: 300 μm, n=9–10). (G) Quantification of the Masson's trichrome-stained fibrotic area in sham-operated, vehicle-treated and BCI-treated hearts at 28 days post-MI (n=9–10 per group). (H) Immunostaining showing TUNEL⁺ cardiomyocytes (CMs) in the infarcted zone in sham-operated, vehicle-treated and BCI-treated heart sections at 7 days post-MI. DAPI was used to stain nuclei, and cTnT was used to stain CMs. Scale bar: 100 μm. (I) Percentage of TUNEL⁺/cTnT⁺ CMs in each group (n=5 per group). One-way ANOVA followed by Dunnett's multiple comparison test; mean±s.e.m.; *P<0.05, **P<0.01, ***P<0.001; ns, not significant.