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Dietary Fish Oil Inhibits Pro-Inflammatory and ER Stress Signalling Pathways in the Liver of Sows during Lactation

机译:日粮鱼油抑制泌乳期母猪肝脏促炎和内质网应激信号通路

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摘要

Lactating sows have been shown to develop typical signs of an inflammatory condition in the liver during the transition from pregnancy to lactation. Hepatic inflammation is considered critical due to the induction of an acute phase response and the activation of stress signaling pathways like the endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR), both of which impair animal´s health and performance. Whether ER stress-induced UPR is also activated in the liver of lactating sows and whether dietary fish oil as a source of anti-inflammatory effects n-3 PUFA is able to attenuate hepatic inflammation and ER stress-induced UPR in the liver of sows is currently unknown. Based on this, two experiments with lactating sows were performed. The first experiment revealed that ER stress-induced UPR occurs also in the liver of sows during lactation. This was evident from the up-regulation of a set of genes regulated by the UPR and numerically increased phosphorylation of the ER stress-transducer PERK and PERK-mediated phosphorylation of eIF2α and IκB. The second experiment showed that fish oil inhibits ER stress-induced UPR in the liver of lactating sows. This was demonstrated by decreased mRNA levels of a number of UPR-regulated genes and reduced phosphorylation of PERK and PERK-mediated phosphorylation of eIF2α and IκB in the liver of the fish oil group. The mRNA levels of various nuclear factor-κB-regulated genes encoding inflammatory mediators and acute phase proteins in the liver of lactating sows were also reduced in the fish oil group. In line with this, the plasma levels of acute phase proteins were reduced in the fish oil group, although differences to the control group were not significant. In conclusion, ER stress-induced UPR is present in the liver of lactating sows and fish oil is able to inhibit inflammatory signaling pathways and ER stress-induced UPR in the liver.
机译:哺乳期母猪已显示出从妊娠到哺乳期过渡期间肝脏中炎症状态的典型体征。由于急性期反应的诱导和内质网(ER)应激诱导的未折叠蛋白反应(UPR)等应激信号通路的激活,肝炎被认为是至关重要的,这两者都会损害动物的健康和性能。 ER应激诱导的UPR是否也在泌乳母猪的肝脏中被激活,以及饮食鱼油是否作为抗炎作用的来源,n-3 PUFA是否能够减轻肝炎症,ER诱导的泌乳性UPR在母猪的肝脏中。目前未知。基于此,对泌乳母猪进行了两次实验。第一个实验表明,泌乳过程中,ER应激诱导的UPR也在母猪肝脏中发生。这从UPR调节的一组基因的上调以及ER应激信号转导物PERK的磷酸化和eIF2α和IκB的PERK介导的磷酸化的数字增加中可以明显看出。第二个实验表明,鱼油可抑制泌乳母猪肝脏中内质网应激诱导的UPR。鱼油组肝脏中许多UPR调控基因的mRNA水平降低和PERK磷酸化以及PERK介导的eIF2α和IκB磷酸化降低证明了这一点。在鱼油组中,泌乳母猪肝脏中各种编码炎症介质和急性期蛋白的核因子-κB调节基因的mRNA水平也降低了。与此相符,鱼油组的急性期蛋白血浆水平降低,尽管与对照组的差异不明显。总之,泌乳母猪的肝脏中存在内质网应激诱导的UPR,鱼油能够抑制肝脏中的炎症信号通路和内质网应激诱导的UPR。

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