Fig. 2.

BCI has no effect on CM proliferation, H₂O₂-induced CM death, CM hypertrophy and coronary vessel regeneration. (A) Released lactate dehydrogenase (LDH) was comparable in neonatal rat ventricular myocytes (NRVMs) treated with DMSO or BCI for 24 h in the presence or absence of H₂O₂ (n=3 per group). (B) Western blots and quantification of Bcl-2 (α-tubulin was used to normalize protein) and p-AKT (AKT was used to normalize protein) in NRVMs treated with DMSO or BCI for 24 h (n=3 per group). (C) Western blots and quantification of H₂O₂-induced cleaved PARP (α-tubulin was used to normalize protein) and cleaved caspase 3 (total caspase 3 was used to normalize protein) in NRVMs treated with DMSO or BCI (n=3 per group). (D) Immunofluorescent staining showing cTnT⁺ and pH3⁺ CMs of sham-operated, vehicle-treated or BCI-treated LV tissues at 7 days after MI (scale bar: 100 μm). (E) Immunofluorescent staining showed that the numbers of either α-actinin⁺ Ki67⁺ or α-actinin⁺ pH3⁺ CMs were comparable in DMSO- and BCI-treated NRVMs (scale bars: 50 μm; n=3 per group). HPF, high-power field. (F) Immunofluorescent staining and statistics for CD31⁺ and α-SMA⁺ vessels of sham-operated, vehicle-treated or BCI-treated LV tissues at 7 days after MI (scale bar: 100 μm; n=3 per group). (G) Wheat germ agglutinin staining and statistics for CM size in sham-operated, vehicle-treated or BCI-treated LV tissues at 28 days after MI (scale bar: 20 μm; n=5 per group). Mean±s.e.m.; ns, not significant.