The biphasic dose effect of lychee (Litchi chinensis Sonn.) pulp phenolic extract on alcoholic liver disease in mice
The biphasic dose effect of lychee (Litchi chinensis Sonn.) pulp phenolic extract on alcoholic liver disease in mice
复制标题
荔枝果肉酚类提取物对小鼠酒精性肝病的双相剂量效应
DOI：
10.1039/c6fo01166g
复制
发表时间：
2017
期刊：
影响因子：
6.1
通讯作者：
Liu D
中科院分区：
文献类型：
--
作者：
Xiao Juan;Zhang Ruifen;Huang Fei;Liu Lei;Deng Yuanyuan;Wei Zhencheng;Zhang Yan;Zhang Mingwei;Liu Dong;Zhang MW;Liu D
荔枝（Litchi chinensis Sonn.）、一种广泛生长于东南亚的亚热带水果，被用作保护肝脏的传统中药。我们先前的研究显示荔枝果肉中的酚类物质对束缚应激引起的肝损伤具有保护活性。本研究旨在探讨荔枝果肉酚类提取物（LPPE）对酒精性肝损伤的保护作用及其机制。小鼠被分成四组，分别给予对照流质饮食（对照组，CON），含4%（w/v）乙醇的流质饮食（乙醇组，EtOH），4%（w/v）含乙醇的液体饲料，补充0.4 g L−1 LPPE（低剂量LPPE补充组，EtOH + L-LPPE），或含4%（w/v）乙醇的液体饮食补充0.8 g L−1 LPPE（高剂量LPPE补充组，EtOH + H-LPPE）持续8周。补充L-LPPE可改善乙醇诱导的肝脏脂肪变性和血清及肝脏中甘油三酯水平的升高，但补充H-LPPE可加重乙醇诱导的肝脏脂肪变性和甘油三酯水平的升高。此外，L-LPPE补充改善了抗氧化状态，减少了核红细胞2相关因子2（Nrf 2）的核转位，并减少了肝脏中Nrf 2靶基因的表达。H-LPPE补充导致抗氧化状态的改善和Nrf 2靶基因的表达减少。L-LPPE抑制脂质合成相关基因的表达，增加脂肪酸β-氧化相关基因的表达。然而，H-LPPE增加了负责脂质合成和摄取的基因的表达，并降低了脂肪酸β-氧化基因的表达。此外，L-LPPE补充有效地降低了血清内毒素水平，并逆转了乙醇诱导的肠道微生物群组成的变化。总的来说，LPPE对乙醇诱导的小鼠肝损伤表现出双相作用，表明适量摄入LPPE或荔枝果肉可能有助于预防和控制酒精性肝病。
Lychee (Litchi chinensis Sonn.), a subtropical fruit grown widely in Southeast Asia, has been used as a traditional Chinese medicine for liver protection. Our previous study showed that phenolics from lychee pulp had hepatoprotective activity against restraint stress-induced liver injury. The present study investigated the protective effects of lychee pulp phenolic extract (LPPE) on ethanol-induced liver injury and the mechanism responsible for these effects. Mice were divided into four groups and subjected to either a control liquid diet (control group, CON), a 4% (w/v) ethanol-containing liquid diet (ethanol group, EtOH), a 4% (w/v) ethanol-containing liquid diet supplemented with 0.4 g L−1 LPPE (low dose LPPE-supplemented group, EtOH + L-LPPE), or a 4% (w/v) ethanol-containing liquid diet supplemented with 0.8 g L−1 LPPE (high dose LPPE-supplemented group, EtOH + H-LPPE) for 8 weeks. The ethanol-induced hepatic steatosis and increases of triglyceride levels in the serum and liver were ameliorated by L-LPPE supplementation but aggravated by H-LPPE supplementation. Moreover, L-LPPE supplementation improved the antioxidant status, reduced the nuclear translocation of nuclear erythroid 2-related factor 2 (Nrf2), and reduced the expression of Nrf2 target genes in the liver. H-LPPE supplementation resulted in the improved antioxidant status and reduced the expression of Nrf2 target genes. Furthermore, L-LPPE suppressed the expression of lipid synthesis genes and increased the expression of fatty acid β-oxidation genes. However, H-LPPE increased the expression of genes responsible for lipid synthesis and uptake and reduced the expression of fatty acid β-oxidation genes. Additionally, L-LPPE supplementation effectively decreased the serum endotoxin level and reversed ethanol-induced alterations in the intestinal microbiota composition. Collectively, LPPE showed biphasic effects on ethanol-induced liver injury in mice, indicating that a moderate intake of LPPE or Litchi pulp could be useful for the prevention and control of alcoholic liver disease.