Abstract
OBJECTIVES: The development and progression of chronic heart failure (CHF), hypertrophy, and remodeling strongly correlate with myocardial inflammation and oxidative stress. S-adenosylmethionine (SAMe), available as a dietary supplement, exerts anti-inflammatory and antioxidant effects. Previous reports show that by regulating angiogenesis and fibrosis, S-adenosyl-L-methionine improves ventricular remodeling. The study objectives were to investigate the cardioprotective effect of SAMe in isoproterenol (ISO)-induced CHF and explore the anti-inflammatory and antioxidant properties of SAMe in this model. METHODOLOGY: After animal ethics permission, CHF was induced using ISO of 10 mg/kg for 14 consecutive days in 24 Wistar rats. There were four groups of six rats in each group: Sham Control, Disease Control (DC), ISO + SAMe 100 mg, and ISO + SAMe 200 mg. The variables assessed were heart to body weight ratio (HW/BW mg/g), bio-distribution of Flourine 18-Fluorodeoxyglucose (18F-FDG) in heart tissue, tumor necrosis factor-α (TNF-α) and glutathione (GSH) levels in heart tissue, histopathology, and positron emission tomography imaging. RESULTS: SAMe in ISO-induced CHF animals showed a significant decrease in the HW/BW compared to DC group (P < 0.001). 18F-FDG uptake was significantly reduced by SAMe in CHF-induced rats compared to DC rats for both doses (P < 0.001). SAMe showed significantly better values of both TNF-α and GSH than the DC group in both doses (P < 0.001). SAMe in both doses showed multifocal necrosis with scarring and minimal inflammatory cells. CONCLUSION: SAMe exerts a cardioprotective effect on ISO-induced CHF in rats because of its antioxidant and anti-inflammatory properties.