Omega-3-fatty acid adds to the protective effect of flax lignan concentrate in pressure overload-induced myocardial hypertrophy in rats via modulation of oxidative stress and apoptosis.

Key Findings:

Cardiac hypertrophy is a hemodynamic response to elevated after load that develops due to pressure or volume overload. Oxidative stress plays a role in inducing myocardial remodeling and hypertrophy in animal models of chronic pressure overload. Myocardial cells can scavenge free radicals effectively by means of antioxidants. A flax lignan concentrate (FLC) has been shown to be myocardial protective. An ALA enriched diet reduced myocardial damage. Secoisolariciresinol diglycoside (SDG) has been shown to be effective in lowering myocardial apoptosis and improving the LV contractile function in rat heart of ischemia–reperfusion injury. In this study, omega 3 fats combined with FLC decreased pressure overload-induced myocardial hypertrophy through enhancing endogenous antioxidants, membrane-bound enzymes, reducing myocardial apoptosis and suppressing inflammation and oxidative stress.

ABSTRACT:

Objective of the present investigation was to study the effect of the flax lignan concentrate (FLC) and Omega-3-fatty acid (O-3-FA) on myocardial apoptosis, left ventricular (LV) contractile dysfunction and electrocardiographic abnormalities in pressure overload-induced cardiac hypertrophy. The rats were divided into five groups such as sham, aortic stenosis (AS), AS + FLC, AS + O-3-FA and AS + FLC + O-3-FA. Cardiac hypertrophy was produced in rats by abdominal aortic constriction. The rats were treated with FLC (400 mg/kg, p.o.), O-3-FA (400 mg/kg, p.o.) and FLC+O-3-FA orally per day for four weeks. The LV function myocardial apoptosis, and oxidative stress were quantified. FLC + O-3-FA treatment significantly reduced hemodynamic changes, improved LV contractile dysfunction, reduced cardiomyocyte apoptosis and cellular oxidative stress. Moreover, it significantly up-regulated the VEGF expression and decreased TNF-alpha level in serum. The histological analysis also revealed that FLC + O-3-FA treatment markedly preserved the cardiac structure and inhibited interstitial fibrosis. In conclusion, FLC + O-3-FA treatment improved LV dysfunction, inhibited cardiomyocyte apoptosis, improved myocardial angiogenesis, conserved activities of membrane-bound phosphatase enzymes and suppressed inflammation through reduced oxidative stress in an additive manner than FLC alone and O-3-FA alone treatment in pressure overload-induced cardiac hypertrophy. Authors Abstract.