1. 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.
- Author
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Ghule AE, Kandhare AD, Jadhav SS, Zanwar AA, and Bodhankar SL
- Subjects
- Animals, Aortic Valve Stenosis complications, Aortic Valve Stenosis metabolism, Aortic Valve Stenosis pathology, Cardiomyopathy, Hypertrophic etiology, Cardiomyopathy, Hypertrophic metabolism, Cardiomyopathy, Hypertrophic pathology, Disease Models, Animal, Drug Therapy, Combination, Fatty Acids, Omega-3 administration & dosage, Hemodynamics drug effects, Lignans administration & dosage, Lignans isolation & purification, Male, Plant Extracts administration & dosage, Plant Extracts isolation & purification, Plant Extracts therapeutic use, Rats, Wistar, Seeds chemistry, Ventricular Function, Left drug effects, Aortic Valve Stenosis drug therapy, Apoptosis drug effects, Cardiomyopathy, Hypertrophic prevention & control, Fatty Acids, Omega-3 therapeutic use, Flax chemistry, Lignans therapeutic use, Oxidative Stress drug effects
- 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 (400mg/kg, p.o.), O-3-FA (400mg/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., (Copyright © 2015 Elsevier B.V. All rights reserved.)
- Published
- 2015
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