The influence of vitamin B6 on cardiac oxidative stress, cardiometabolic and histological markers in monocrotaline-induced heart failure in Wistar albino rats

Abstract

Introduction/Aim: Heart failure (HF) induced by monocrotaline (MCT) is common in the pulmonary arterial vessels remodeling mechanisms with increased pulmonary resistance and oxidative stress markers. The purpose of this study was to validate the hypothesis that the treatment with vitamin B6 could affect HF by modulating cardiometabolic and oxidative stress biomarkers, and the structure of the rat heart. Material and Methods: Male Wistar albino rats were divided into 3 groups: blank solution-exposed control (C physiological saline 1ml/kg 28 days ip., n=8), B6 (vitamin B6 7mg/kg/day 28 days ip., n=8), and MCT+B6 (MCT 50mg/ kg once ip. plus vitamin B6 7mg/kg/day 28 days ip., n=8). Results: The four-week vitamin B6 treatment significantly affected certain biochemical parameters. The activity of key antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (GPX) did not change, whereas the total glutathione (GSH) was significantly decreased in the MCT+B6 group. This was followed by a slightly decreased level of the total glutathionylation observed in the MCT+B6 group. The parameters of protein oxidative damage (reactive carbonyl derivates, thiol groups and nitrotyrosine) did not significantly change in the MCT+B6 group. An increasing trend in RV and LV wall thickness was observed in the MCT+B6 compared to the C group, as well as in Ki67 and PCNA positivity. Conclusion: The four-week treatment with vitamin B6 significantly affected certain biomarkers. The activity of SOD and nitrotyrosine content did not change, while GPX activity, total glutathione and total glutathionylation level were decreased in the MCT+B6 group. We observed an increase in RV and LV wall thickness in the MCT+B6 group compared to the C group, as well as in Ki67 and PCNA positivity.