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Pterostilbene reduces oxidative stress, prevents hypertrophy and preserves systolic function of right ventricle in cor pulmonale model
Author(s) -
Santos Lacerda Denise,
Türck Patrick,
Gazzi de LimaSeolin Bruna,
Colombo Rafael,
Duarte Ortiz Vanessa,
Poletto Bonetto Jéssica Hellen,
CamposCarraro Cristina,
Bianchi Sara Elis,
BellóKlein Adriane,
Linck Bassani Valquiria,
Sander da Rosa Araujo Alex
Publication year - 2017
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/bph.13948
Subject(s) - ventricle , oxidative stress , medicine , afterload , pulmonary hypertension , diastole , endocrinology , muscle hypertrophy , pterostilbene , oxidative phosphorylation , cardiology , pharmacology , chemistry , biochemistry , blood pressure , resveratrol
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.