TY - JOUR
T1 - Pterostilbene reduces oxidative stress, prevents hypertrophy and preserves systolic function of right ventricle in cor pulmonale model
AU - dos Santos Lacerda, Denise
AU - Türck, Patrick
AU - Gazzi de Lima-Seolin, Bruna
AU - Colombo, Rafael
AU - Duarte Ortiz, Vanessa
AU - Poletto Bonetto, Jéssica Hellen
AU - Campos-Carraro, Cristina
AU - Bianchi, Sara Elis
AU - Belló-Klein, Adriane
AU - Linck Bassani, Valquiria
AU - Sander da Rosa Araujo, Alex
N1 - Publisher Copyright:
© 2017 The British Pharmacological Society.
PY - 2017
Y1 - 2017
N2 - Background and Purpose: In cor pulmonale, the increased afterload imposed on the right ventricle (RV) generates a maladaptive response, impairing the contractile cardiac function. Oxidative mechanisms play an important role in the pathophysiology and progression of this disease. The administration of pterostilbene (PTS), a phytophenol with antioxidant potential, may represent a therapeutic option. In the present study, we evaluated the effect of PTS complexed with hydroxypropyl-β-cyclodextrin (HPβCD) on hypertrophy, contractile function and oxidative parameters in the RV of rats with pulmonary hypertension, induced by the administration of monocrotaline (MCT). Experimental Approach: The rats received daily doses of the PTS : HPβCD complex at 25, 50 or 100 mg·kg−1, p.o., for 14 days. The diastolic function, E/A ratio, and systolic function, shortening fraction, fractional area change (FAC) and tricuspid annular plane systolic excursion (TAPSE) of the RV were determined by echocardiography. Key Results: The PTS : HPβCD complex reduced the production of NADPH oxidase-dependent superoxide anions and oxidative stress in the RV of MCT-treated rats in a dose-dependent manner. At higher doses it prevented the reduction in FAC and TAPSE in MCT-treated animals. Conclusions and Implications: The PTS : HPβCD complex prevented the maladaptative remodelling and protected systolic function in the RV of rats with pulmonary hypertension. These cardioprotective mechanisms may be related, in part, to the antioxidant potential of PTS, favoured by the increased p.o. bioavailability promoted by the presence of HPβCD in the complex.
AB - Background and Purpose: In cor pulmonale, the increased afterload imposed on the right ventricle (RV) generates a maladaptive response, impairing the contractile cardiac function. Oxidative mechanisms play an important role in the pathophysiology and progression of this disease. The administration of pterostilbene (PTS), a phytophenol with antioxidant potential, may represent a therapeutic option. In the present study, we evaluated the effect of PTS complexed with hydroxypropyl-β-cyclodextrin (HPβCD) on hypertrophy, contractile function and oxidative parameters in the RV of rats with pulmonary hypertension, induced by the administration of monocrotaline (MCT). Experimental Approach: The rats received daily doses of the PTS : HPβCD complex at 25, 50 or 100 mg·kg−1, p.o., for 14 days. The diastolic function, E/A ratio, and systolic function, shortening fraction, fractional area change (FAC) and tricuspid annular plane systolic excursion (TAPSE) of the RV were determined by echocardiography. Key Results: The PTS : HPβCD complex reduced the production of NADPH oxidase-dependent superoxide anions and oxidative stress in the RV of MCT-treated rats in a dose-dependent manner. At higher doses it prevented the reduction in FAC and TAPSE in MCT-treated animals. Conclusions and Implications: The PTS : HPβCD complex prevented the maladaptative remodelling and protected systolic function in the RV of rats with pulmonary hypertension. These cardioprotective mechanisms may be related, in part, to the antioxidant potential of PTS, favoured by the increased p.o. bioavailability promoted by the presence of HPβCD in the complex.
UR - http://www.scopus.com/inward/record.url?scp=85029544436&partnerID=8YFLogxK
U2 - 10.1111/bph.13948
DO - 10.1111/bph.13948
M3 - Article
C2 - 28703274
AN - SCOPUS:85029544436
SN - 0007-1188
VL - 174
SP - 3302
EP - 3314
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
IS - 19
ER -