Ethanol Extract of Liriope platyphylla Root Attenuates Non-Alcoholic Fatty Liver Disease in High-Fat Diet-Induced Obese Mice via Regulation of Lipogenesis and Lipid Uptake.

Ethanol Extract of Liriope platyphylla Root Attenuates Non-Alcoholic Fatty Liver Disease in High-Fat Diet-Induced Obese Mice via Regulation of Lipogenesis and Lipid Uptake.
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阔叶山麦冬根乙醇提取物通过调节脂肪生成和脂质摄取减轻高脂饮食诱导的肥胖小鼠的非酒精性脂肪性肝病

DOI:
10.3390/nu13103338
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发表时间:
2021-09-24
期刊:
影响因子:
5.9
通讯作者:
Jun HS
Jun HS
中科院分区:
医学2区
文献类型:
--
作者:
Le TNH;Choi HJ;Jun HS

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非酒精性脂肪性肝病(NAFLD)是一种常见的代谢紊乱,导致肝脏中脂质过度积聚,是终末期肝病的主要原因。麦冬是一种草药,长期以来一直用于治疗咳嗽,肥胖和糖尿病。然而,尚未研究过宽叶山麦冬对NAFLD的影响。本研究旨在探讨麦冬根乙醇提取物(LPE)对高脂饮食(HFD)诱导的肥胖小鼠肝脏脂质蓄积的影响。对6周龄C57 BL/6雄性小鼠喂食HFD 8周,然后经口灌胃给予LPE(100或250 mg/kg/天)再处理8周。250 mg/kg LPE处理的HFD组的体重增加和肝脏重量显著低于溶剂处理的HFD组。肝脏切片的组织学分析表明,与媒介物处理相比,LPE处理减少了脂质积累。LPE处理的HFD组的血清总胆固醇、AST和ALT水平与溶媒处理的HFD组相比显著降低。在体内和体外,LPE显著降低参与脂肪生成的SREBP 1、ACC、p-ACC、FAS和SCD 1以及参与脂肪酸摄取的PPARγ、CD 36/FAT和FATP 5的蛋白表达水平。因此,LPE可以通过抑制脂肪生成和脂肪酸摄取来减少脂质积累,从而减轻HFD诱导的NAFLD。
Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disorder that causes excess lipid accumulation in the liver and is the leading cause of end-stage liver disease. Liriope platyphylla is a medicinal herb that has long been used to treat cough, obesity, and diabetes. However, the effect of Liriope platyphylla on NAFLD has not been studied. The aim of this study was to investigate the effect of Liriope platyphylla root ethanolic extract (LPE) on hepatic lipid accumulation in high-fat diet (HFD)-induced obese mice. Six-week-old C57BL/6 male mice were fed a HFD for 8 weeks and then treated with LPE (100 or 250 mg/kg/day) by oral gavage for another 8 weeks. Body weight gain and liver weight were significantly lower in the 250 mg/kg LPE-treated HFD group than in the vehicle-treated HFD group. Histological analysis of liver sections demonstrated that LPE treatment reduced lipid accumulation compared to the vehicle treatment. The serum total cholesterol, AST, and ALT levels significantly decreased in the LPE-treated HFD group compared to those in the vehicle-treated HFD group. The LPE significantly decreases the protein expression levels of SREBP1, ACC, p-ACC, FAS, and SCD1, which are involved in lipogenesis, and PPARγ, CD36/FAT, and FATP5, which are involved in fatty acid uptake, both in vivo and in vitro. Thus, LPE may attenuate HFD-induced NAFLD by decreasing lipid accumulation by inhibiting lipogenesis and fatty acid uptake.
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