Curcumin, A Natural P300-Specific Histone Acetyltransferase Inhibitor, Prevents the Development of Hypertension-Induced Left Ventricular Hypertrophy in Rats

Objective: We found that curcumin, a natural compound that inhibits p300 histone acetyltransferase activity, prevents the deterioration of the systolic function in rat heart failure models in vivo. To solve whether curcumin prevents the development of hypertension-induced left ventricular hypertrophy (LVH) at an early stage of hypertension, we have utilized a salt-sensitive Dahl rat (DS) model of hypertension. Methods: We randomized 6-week-old DS (n=19) and control salt-resistant Dahl rats (DR, n=10) to a curcumin or the vehicle group. Then, these rats were given a high-salt diet and subjected to daily oral treatment with 50 mg/kg/day of curcumin or its vehicle for 5 weeks. Results: There were no differences between curcumin and vehicle in any data examined before treatment. At 11 weeks of age, the LV wall thickness, LV mass, and LV fractional shortening were significantly higher in DS compared with DR, and the LV systolic and diastolic dimensions were significantly smaller in DS than DR. Curcumin treatment significantly (p<0.0001) decreased the LV wall thickness (curcumin:1.4 mm, Veh:2.0 mm) and LV mass (curcumin:0.76 g/m2, vehicle:1.06 g/m2) in DS but not DR. However, LV fractional shortening in DS was similar between the two groups. Conclusions: Curcumin inhibits the development of hypertension-induced concentric LVH without affecting the systolic function. Thus, this compound might be applicable to patients with early-stages hypertensive heart diseases.