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Rumen-derived lipopolysaccharide provoked inflammatory injury in the liver of dairy cows fed a high-concentrate diet

机译:瘤胃来源的脂多糖引起高浓度饮食的奶牛肝脏炎症性损伤

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摘要

Rumen-derived lipopolysaccharide (LPS) is translocated from the rumen into the bloodstream when subacute ruminal acidosis (SARA) occurs following long-term feeding with a high-concentrate (HC) diet in dairy cows. The objective of this study was to investigate the mechanism of inflammatory responses in the liver caused by HC diet feeding. We found that SARA was induced in dairy cows when rumen pH below 5.6 lasted for at least 3 h/d with HC diet feeding. Also, the LPS levels in the portal and hepatic veins were increased significantly and hepatocytes were impaired as well as the liver function was inhibited during SARA condition. Meanwhile, the mRNA expression of immune genes including TNF receptor associated factor 6 (TRAF6), nuclear factor-kappa B (NF-κB), p38 mitogen-activated protein kinase (MAPK), extracellular regulated protein kinases (ERK) MAPK, Interleukin-1 (IL-1) and serum amyloid A (SAA) in the liver were significantly increased in SARA cows. Moreover, the phosphorylation level of NF-κB p65 and p38 MAPK proteins in the liver and the concentration of Tumor Necrosis Factor (TNF-α), Interleukin-1β (IL-1β) and Interleukin-6 (IL-6) in peripheral blood were obviously increased under SARA condition. In conclusion, the inflammatory injury in the liver caused by LPS that traveled from the digestive tract to the liver through the portal vein after feeding with a HC diet.
机译:在奶牛长期饲喂高浓度(HC)饮食后发生亚急性瘤胃酸中毒(SARA)时,瘤胃来源的脂多糖(LPS)从瘤胃转移到血液中。这项研究的目的是研究高脂饮食喂养引起的肝脏炎症反应的机制。我们发现当HC饮食饲喂瘤胃pH低于5.6时,SARA在乳牛中被诱导持续至少3小时/天。此外,在SARA状态下,门静脉和肝静脉中的LPS水平显着增加,肝细胞受损,肝功能受到抑制。同时,免疫基因的mRNA表达包括TNF受体相关因子6(TRAF6),核因子-κB(NF-κB),p38丝裂原活化蛋白激酶(MAPK),细胞外调节蛋白激酶(ERK)MAPK,白介素- SARA奶牛肝脏中的1(IL-1)和血清淀粉样蛋白A(SAA)显着增加。此外,肝脏中NF-κBp65和p38 MAPK蛋白的磷酸化水平以及外周血中肿瘤坏死因子(TNF-α),白介素-1β(IL-1β)和白介素-6(IL-6)的浓度在SARA条件下明显增加。总而言之,LPS引起的肝炎性损伤是在喂食HC饮食后从消化道通过门静脉到达肝脏的。

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