Hepatoprotective effect of mulberry water extracts on ethanol-induced liver injury via anti-inflammation and inhibition of lipogenesis in C57BL/6J mice
Hepatoprotective effect of mulberry water extracts on ethanol-induced liver injury via anti-inflammation and inhibition of lipogenesis in C57BL/6J mice
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DOI：
10.1016/j.fct.2013.10.011
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发表时间：
2013-12-01
影响因子：
4.3
通讯作者：
Wang, Chau-Jong
中科院分区：
文献类型：
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作者：
Tang, Chang-Chieh;Huang, Hui-Pei;Wang, Chau-Jong
许多植物提取物及其生物活性物质被公认为具有抗常见酒精性肝损伤的化学保护剂的潜力。本研究探讨了桑葚水提取物（MWE）对小鼠酒精性肝损伤的预防作用。MWE含有多种营养成分和生物活性物质，包括15种多酚类和花青素类化合物。组织病理学、免疫组化、抗氧化防御和促炎介质等指标表明MWE对酒精性肝损伤具有抑制作用。血浆和肝脏含量分析表明，MWE抑制肝损伤生物标志物（AST，ALT和ALP），甘油三酯（TG）和胆固醇（TC）的水平。此外，MWE处理降低了脂质合成相关蛋白的表达，增加了p-AMPK/AMPK比值和PPAR-cc，激活了脂肪酸氧化和通过微粒体甘油三酯转移蛋白（MTP）的输出以及肉毒碱棕榈酰转移酶-1（CPT 1）。这些结果表明，MWE通过激活AMPK和PPAR-alpha信号防止酒精诱导的肝损伤。这可能是由多种途径介导的，包括减少脂质积累和脂质合成，增加脂肪酸转运和脂肪酸氧化反应，减少氧化应激和促进抗炎。皇冠版权所有（C）2013由爱思唯尔有限公司出版。保留所有权利。
Many plant extracts and their bioactive substances are well recognized for their potential to exert as chemoprotective agents against common alcoholic liver injury. In this study, the effects of Mulberry water extracts (MWE) treatment in the prevention of alcohol-induced liver injury were investigated in mice. MWE contain many nutrients and bioactive substances, including fifteen types of polyphenols and anthocyanin compounds. The parameters of histopathology, immunohistochemistry, antioxidant defense and proinflammatory mediator demonstrated the inhibitory effect of MWE on alcohol-induced liver injury. Plasma and hepatic content analysis showed that MWE inhibited the levels of liver injury biomarkers (AST, ALT and ALP), triglyceride (TG) and cholesterol (TC). Furthermore, treatment with MWE lessened the expression of lipid synthesis-related proteins, increased the p-AMPK/AMPK ratio and PPAR-cc Fatty acid oxidation and export via microsomal triglyceride transfer protein (MTP) were both activated as well as carnitine palmitoyltransferase-1 (CPT1). These results suggested that MWE prevents alcohol-induced liver injury through the activation of the AMPK and PPAR-alpha signal. This may be mediated by multiple pathways, including reduced lipid accumulation and lipid synthesis, increased fatty acid transport and fatty acid oxidation responses, decreased oxidative stress and facilitated anti-inflammation. Crown Copyright (C) 2013 Published by Elsevier Ltd. All rights reserved.