The dietary compound curcumin inhibits p300 histone acetyltransferase activity and prevents heart failure in rats
J. Clin. Invest. Tatsuya Morimoto, et al. 118:868 doi:10.1172/JCI33160 [Go to this article.]

Figure 1
Curcumin inhibits PE-induced hypertrophic responses in cardiomyocytes. (A and B) Primary cardiomyocytes from neonatal rats were stimulated with saline or 30 μM PE in the presence of curcumin (10 μM in A and 5 or 10 μM in B) or a corresponding amount of its vehicle (DMSO) as a control for 48 hours. (A) These cells were subjected to immunocytochemistry using the primary antibody against cardiac MHC followed by staining with a secondary antibody conjugated with peroxidase (brown signals). Scale bar: 10 μm. (B) Myocardial cell-surface area was measured as described in Methods. Values in each group are mean ± SEM (μm) from 50 cells. (C and D) Cardiomyocytes were transfected with 0.5 μg of pANF-luc (C) or pβ-MHCluc (D) and 0.0025 μg of pRL-SV40. Then, these cells were stimulated with saline or 30 μM PE in the presence of curcumin or a corresponding amount of its vehicle for 48 hours. The relative promoter activities were calculated from the ratio of firefly Luc activity to sea pansy Luc activity. The data shown are mean ± SEM from 3 independent experiments, each carried out in duplicate.