4.7 Article

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

期刊

INTERNATIONAL IMMUNOPHARMACOLOGY
卷 28, 期 1, 页码 751-763

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2015.08.005

关键词

Antioxidants; Apoptosis; Cardiac hypertrophy; Electrocardiography; Flax lignan concentrate; Omega-3-fatty acid; ROS; TNF-alpha; VEGF

资金

  1. All India Council for Technical and Education (AICTE), India [RID/NDF/2009/10]
  2. Indian Council for Agriculture Research under the National Agriculture Innovation Project, entitled A value chain on linseed: Processing and value addition for profitability

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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 PLC + O-3-FA orally per day for four weeks. The LV function, myocardial apoptosis, and oxidative stress were quantified. PLC + 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 PLC + 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 PLC alone and O-3-FA alone treatment in pressure overload-induced cardiac hypertrophy. (C) 2015 Elsevier B.V. All rights reserved.

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