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首页> 外文期刊>International immunopharmacology >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
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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

机译：Omega-3-脂肪酸增加了通过调节氧化应激和细胞凋亡的大鼠压力过载诱导的心肌肥厚的亚麻拉链浓缩物的保护作用

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摘要

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.
机译：本研究的目的是研究亚麻木香料浓缩物（FLC）和ω-3-脂肪酸（O-3-FA）对心肌细胞凋亡，左心室（LV）收缩功能障碍和心电图异常在压力过载中的影响 - 诱导心脏肥大。将大鼠分为五组，如假，主动脉狭窄（AS），AS + FLC，AS + O-3-FA和AS + FLC + O-3-FA。通过腹主动脉收缩在大鼠中产生心脏肥大。将大鼠用FLC（400mg / kg，p.O.），O-3-FA（400mg / kg，P.O）和PLC + O-3-FA每天处理四周。量化了LV功能，心肌细胞凋亡和氧化应激。 PLC + O-3-FA治疗显着降低了血液动力学变化，改善了LV收缩功能障碍，减少心肌细胞凋亡和细胞氧化应激。此外，它显着上调VEGF表达并降低了血清中的TNF-α水平。组织学分析还显示PLC + O-3-FA治疗显着保留了心脏结构并抑制间质纤维化。总之，FLC + O-3-FA治疗改善了LV功能障碍，抑制心肌细胞凋亡，改善心肌血管生成，膜结合的磷酸酶的保守活性，通过单独的PLC降低氧化应激，通过降低氧化应激和o-3- FA单独治疗压力过载诱导的心脏肥大。 （c）2015 Elsevier B.v.保留所有权利。

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