| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2540515 | International Immunopharmacology | 2015 | 13 Pages |
•Cardiac hypertrophy is an important cause of cardiac dysfunction and heart failure•FLC and Omega combination treatment reduced the progression of cardiac hypertrophy•Concomitant treatment significantly improved the ECG changes and LV function•Combination treatment also reduced TNF-α level and up-regulated VEGF mRNA expression•Effect is mediated via increased angiogenesis and decreased apoptosis along with ROS
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.
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