Heart failure (HF) is one of the major cardiovascular causes of death worldwide. In this study, we explored the effects of folic acid (FA) on cardiometabolic, oxidative stress-biomarker changes and the activity of proliferation marker Ki67 in monocrotaline-induced HF. The research was conducted during a 4-week period, using 5 experimental groups (8 animals/group): blank solution-exposed controls (C1 physiological saline 1ml/kg one day; C2 physiological saline 1ml/kg 28 days), MCT-induced HF (MCT 50mg/kg), FA (FA 5mg•kg-1•day-1) and MCT+FA (MCT 50mg/kg, FA 5mg•kg-1•day-1). Superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities together with total glutathione and parameters of oxidative damage of proteins were determined in cardiac tissue, as well as cardiometabolic parameters in plasma or serum. The total glutathionylation was determined by Western blot, and proliferation marker Ki67 was assessed by immunohistochemistry. The right ventricular wall hypertrophy and Ki67 positivity, accompanied with significant increase of troponin T has been shown in MCT-induced HF. The antioxidant effect of folic acid was reflected through SOD activity, reduced Ki67 positivity in RV wall and slightly decreased total glutathionylation level. Folic acid intraperitoneal injection modulated oxidative stress, and reduced cardiomyocyte proliferation in RV wall.

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PubMed