Preventive effects of (-) epicatechin on tachycardia, cardiac hypertrophy, and nuclear factor- κB inflammatory signaling pathway in isoproterenol-induced myocardial infarcted rats.

Myocardial infarction (MI) is a life-threatening condition. No studies were conducted earlier on the effects of (-) epicatechin (EC) on tachycardia, cardiac hypertrophy, and inflammation in MI. Hence, the preventive effects of EC on tachycardia, cardiac hypertrophy, and nuclear factor- κB inflammatory signaling pathway in experimental MI were appraised. This investigation included 4 groups of 24 male albino Wistar rats. Group:1. Normal control, Group: 2. EC (20 mg/kg body weight), Group: 3. Isoproterenol (100 mg/kg body weight), Group:4. EC (20 mg/kg body weight) + Isoproterenol (100 mg/kg body weight). MI was created in rats by isoproterenol (100 mg/kg body weight). The heart rate, heart weight, plasma myoglobin, serum cardiac troponin I, heart conjugated dienes, serum high-sensitivity C-reactive protein, and plasma total homocysteine were considerably (P < 0.05) raised in isoproterenol-induced myocardial infarcted rats. Further, reverse transcription-polymerase chain reaction study revealed a considerable (P < 0.05) increase in the expressions of heart pro-inflammatory cytokines such as nuclear factor- κB, tumor necrosis factor-α, interleukin-1β, interleukin-6, and a considerable (P < 0.05) decrease in anti-inflammatory cytokine gene, interleukin-10 in myocardial infarcted rats. Non-enzymatic antioxidants such as vitamin C, and vitamin E were considerably (P < 0.05) lessened in the heart. EC (20 mg/kg body weight) pre-treatment orally, daily, for 3 weeks prevented all changes in the above-mentioned functional, structural, biochemical, and molecular parameters investigated and improved cardiac function. The possible mechanisms are EC's anti-tachycardial, anti-cardiac hypertrophic, antioxidant, and anti-inflammatory effects.