Sulforaphane improves redox homeostasis and right ventricular contractility in a model of pulmonary hypertension.

Pulmonary arterial hypertension (PAH) is characterized by increased pulmonary vascular resistance, imposing overload on the right ventricle (RV) and imbalance of redox state. Our study investigated the influence of treatment with sulforaphane (SFN), found in cruciferous vegetables, on right ventricle (RV) remodeling and redox homeostasis in monocrotaline-induced pulmonary arterial hypertension (PAH). Male Wistar rats were separated into four groups: control (CTR); control + sulforaphane (CTR + SFN); monocrotaline (MCT); monocrotaline + sulforaphane (MCT + SFN). PAH induction was implemented by a single dose of MCT (60 mg/kg i.p.). Treatment with SFN (2.5 mg/kg/day i.p.) started on the 7th day after the MCT injection and persisted for 2 weeks. After 21 days of PAH induction, echocardiography, hemodynamic, and oxidative stress evaluation were performed. MCT group showed increase in RV hypertrophy, RV systolic area, RV systolic, mean pulmonary artery pressure (mPAP), and pulmonary vascular resistance (PVR), while exhibited a decrease in RV outflow tract AT/ET ratio, RV fractional shortening and tricuspid annular plane systolic excursion (TAPSE) compared to CTR (P<0.05). SFN-treated PAH attenuated detrimental changes in TPSE, mPAP, and PVR parameters. Catalase and GSH/GSSG ratio were diminished in MCT compared to CTR (P<0.05). SFN increased catalase and normalized GSH/GSSG ratio to control levels (P<0.05). Data express a benefit of SFN treatment on the cardiac function of rats with PAH associated with the cellular redox state.