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Water Extract of Curcuma longa L. Ameliorates Non-Alcoholic Fatty Liver Disease

机译:姜黄提取物可改善非酒精性脂肪性肝病

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摘要

Our aim was to investigate whether hot water extract (CLW) of L. could prevent non-alcoholic fatty liver disease (NAFLD). HepG2 cells were treated with free fatty acid (FFA) mixture (oleic acid: palmitic acid, 2:1) for 24 h to stimulate in vitro fatty liver. In addition, C57BL/6 mice were fed 60 kcal% high-fat (HF) diet for eight weeks to induce fatty liver in vivo. Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) productions were increased by FFA and HF-diet, but supplementation with CLW significantly decreased these levels. CLW treatment ameliorated antioxidant activities that were suppressed by exposure to the FFA and HF-diet. Cluster of differentiation 36 (CD36) and fatty acid transport proteins (FATP2 and FATP5) were increased in HF-diet groups, while CLW suppressed their expression levels. Moreover, sterol regulatory element-binding protein-1c (SREBP-1c), acetyl-coenzyme A carboxylase (ACC), and fatty acid synthase (FAS) expression levels were down-regulated in the CLW groups compared to HF-diet groups. On the other hand, 5′ adenosine monophosphate-activated protein kinase (AMPK), Peroxisome proliferator-activated receptor alpha (PPAR-α), and carnitine palmitoyltransferase 1 (CPT-1) expressions were up-regulated in the CLW groups. HF-diet fed mice showed high hepatic triglycerides (TG) content compared to the normal diet mice. However, the administration of CLW restored the hepatic TG level, indicating an inhibitory effect against lipid accumulation by CLW. These results suggest that CLW could be a potentially useful agent for the prevention of NAFLD through modulating fatty acid uptake.
机译:我们的目的是调查L.的热水提取物(CLW)是否可以预防非酒精性脂肪性肝病(NAFLD)。用游离脂肪酸(FFA)混合物(油酸:棕榈酸,2:1)处理HepG2细胞24小时,以刺激体外脂肪肝。另外,给C57BL / 6小鼠喂食60kcal%的高脂(HF)饮食八周以在体内诱导脂肪肝。 FFA和HF饮食增加了细胞内活性氧(ROS)和丙二醛(MDA)的产生,但补充CLW则明显降低了这些水平。 CLW处理改善了通过暴露于FFA和HF饮食中而被抑制的抗氧化活性。 HF饮食组中分化簇36(CD36)和脂肪酸转运蛋白(FATP2和FATP5)的簇增加,而CLW抑制它们的表达水平。此外,与HF-饮食组相比,CLW组中的固醇调节元件结合蛋白-1c(SREBP-1c),乙酰辅酶A羧化酶(ACC)和脂肪酸合酶(FAS)表达水平下调。另一方面,CLW组中5'腺苷单磷酸激活蛋白激酶(AMPK),过氧化物酶体增殖物激活受体α(PPAR-α)和肉碱棕榈酰转移酶1(CPT-1)的表达上调。与正常饮食小鼠相比,HF饮食喂养的小鼠显示出较高的肝甘油三酸酯(TG)含量。然而,CLW的施用恢复了肝TG水平,表明对CLW对脂质蓄积的抑制作用。这些结果表明,CLW可能是通过调节脂肪酸摄入来预防NAFLD的潜在有用药物。

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