Pathophysiology Program, Biomedical Sciences Institute, Faculty of Medicine, Universidad de Chile, Santiago, Chile.
Cell Biochem Funct. 2014 Apr;32(3):274-81. doi: 10.1002/cbf.3012. Epub 2013 Oct 24.
Currently, controversial clinical data about the protective effects in the consumption of n-3 polyunsaturated fatty acids (PUFAs) in ischaemic heart diseases exist. Improved myocardial resistance to ischaemia-reperfusion (IR) injury results in non-lethal myocardial infarction, which is a relevant factor in the myocardial function. We hypothesized that chronic supplementation with PUFAs reduced infarct size (IS) and induced an improvement on oxidative stress-related parameters in IR model. Rats were supplemented with two doses of PUFAs D1 (n = 7) (0.6 g kg(-1) d(-1) ) and D2 (n = 7) (1.2 g kg(-1) d(-1) ) for 8 weeks. Control group (n = 7) received only standard diet. In ex vivo model, all rat hearts were subjected to 30 min of global ischaemia followed by 120 min of reperfusion. The IS and left ventricular function were assessed. Lipid peroxidation, reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio and antioxidant enzyme activity were measured in the whole heart. The results show a reduction in IS in a dose-dependent manner with PUFAs D1 (30.6%) and D2 (48.5%) and higher values of left ventricular developed pressure, at the end of the reperfusion, for each dose, respectively (p < 0.05). The two PUFAs groups showed higher values of GSH/GSSG ratio and lipid peroxidation, and higher values of activity of antioxidant enzymes catalase, superoxide dismutase and glutathione peroxidase at basal condition (p < 0.05). At the end of reperfusion, the GSH/GSSG ratio and antioxidants enzyme activity did not show a significant drop in their values (p > 0.05). These findings suggested that the supplementation with PUFAs induces cardioprotection against IR injury, associated with reinforcement of the antioxidant defense system.
目前,关于 n-3 多不饱和脂肪酸(PUFAs)在缺血性心脏病中的保护作用存在争议的临床数据。改善心肌对缺血再灌注(IR)损伤的抵抗力会导致非致命性心肌梗死,这是心肌功能的一个相关因素。我们假设慢性补充 PUFAs 会减少梗死面积(IS)并改善 IR 模型中与氧化应激相关的参数。大鼠补充两种剂量的 PUFAs D1(n = 7)(0.6 g kg-1 d-1)和 D2(n = 7)(1.2 g kg-1 d-1)8 周。对照组(n = 7)仅接受标准饮食。在离体模型中,所有大鼠心脏均经历 30 分钟的整体缺血,然后再进行 120 分钟的再灌注。评估 IS 和左心室功能。在整个心脏中测量脂质过氧化、还原型谷胱甘肽(GSH)/氧化型谷胱甘肽(GSSG)比和抗氧化酶活性。结果显示,PUFAs D1(30.6%)和 D2(48.5%)呈剂量依赖性降低 IS,并且每个剂量的左心室发展压在再灌注结束时均升高(p < 0.05)。两组 PUFAs 均表现出更高的 GSH/GSSG 比和脂质过氧化水平,以及更高的抗氧化酶活性,如过氧化氢酶、超氧化物歧化酶和谷胱甘肽过氧化物酶(p < 0.05)。在再灌注结束时,GSH/GSSG 比和抗氧化酶活性的数值没有明显下降(p > 0.05)。这些发现表明,PUFAs 的补充可诱导对 IR 损伤的心脏保护作用,与抗氧化防御系统的增强有关。