首页> 外文期刊>The British Journal of Nutrition >Linoleic acid, α-linolenic acid and enterolactone affect lipid oxidation and expression of lipid metabolism and antioxidant-related genes in hepatic tissue of dairy cows
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Linoleic acid, α-linolenic acid and enterolactone affect lipid oxidation and expression of lipid metabolism and antioxidant-related genes in hepatic tissue of dairy cows

机译:亚油酸,α-亚麻酸和肠内烯酮影响乳制奶牛肝组织中脂质氧化和脂质代谢和抗氧化相关基因的表达

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Although beneficial effects have been attributed to PUFA supplementation in high-yielding dairy cows, diets rich in PUFA may also increase oxidative stress in tissues such as the liver. To fully exploit the health benefits of PUFA, we believe that the addition of natural antioxidants could help in preventing oxidative damage. Using an in vitro precision-cut liver slices (PCLS) tissue culture system, we investigated the effects of different linoleic acid (LA, n-6):α-linolenic acid (ALA, n-3) ratios (LA:ALA ratio of 4, LA:ALA ratio of 15 and LA:ALA ratio of 25) in the presence or absence of the antioxidant enterolactone (ENL) on (1) the mRNA abundance of genes with key roles in hepatic lipid metabolism, oxidative stress response and inflammatory processes, (2) oxidative damages to lipids and proteins and (3) superoxide dismutase activity in early-lactating dairy cows. The addition of LA and ALA to PCLS culture media increased oxidative damage to lipids as suggested by higher concentrations of thiobarbituric acid reactive substances and increased the expression of nuclear factor erythroid 2-related factor 2 target genes. The addition of ENL was effective in preventing lipid peroxidation caused by LA and ALA. Transcript abundance of sterol regulatory element-binding transcription factor 1 and its lipogenic target genes acetyl-CoA carboxylase α, fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD) was decreased with LA and ALA, whereas ENL decreased FASN and SCD gene expression. Our results show that addition of LA and ALA to PCLS culture media lowers hepatic lipogenic gene expression and increases oxidative damages to lipids. On the other hand, addition of ENL prevents oxidative damages provoked by these PUFA.
机译:虽然有益效果已归因于高产奶牛的PUFA补充,但富含PUFA的饮食也可能增加肝脏等组织中的氧化应激。为了充分利用PUFA的健康益处,我们认为添加天然抗氧化剂可能有助于预防氧化损伤。使用体外精密切割肝脏切片(PCLS)组织培养系统,我们研究了不同亚油酸(LA,N-6):α-亚麻酸(ALA,N-3)比的影响(LA:ALA比4,LA:ALA比率为15和La:ALA比例为25)在抗氧化剂肠内酮(ENL)的存在或不存在(1)肝脂代谢中具有关键作用的MRNA丰富,氧化应激反应和炎症方法,(2)对脂质和蛋白质的氧化损伤和(3)早期哺乳酸奶牛中的超氧化物歧化酶活性。添加La和Ala至PCLS培养基对脂质的氧化损伤增加,如较高浓度的硫氨基碱酸反应物质所提出的,并增加核因子红外2相关因子2靶基因的表达。增强的添加是有效预防由La和Ala引起的脂质过氧化。甾醇调节元素结合转录因子1及其脂肪酸靶基因乙酰-CoA羧化酶α,脂肪酸合酶(FasN)和硬脂酰基-CoA去饱和酶(SCD)的转录物丰度与La和Ala降低,而INL减少了FasN和SCD基因表达。我们的结果表明,La和Ala对PCLS培养基的添加降低了肝脂肪生成的基因表达,并增加了脂质的氧化损伤。另一方面,添加IN的添加防止这些PUFA引发的氧化损伤。

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