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山西老陈醋通过激活 Nrf2 介导的抗氧化和抑制 TLR4 诱导的炎症反应来预防酒精性肝损伤。

Shanxi Aged Vinegar Protects against Alcohol-Induced Liver Injury via Activating Nrf2-Mediated Antioxidant and Inhibiting TLR4-Induced Inflammatory Response.

机构信息

State Key Laboratory of Food Nutrition and Safety, Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, Tianjin Engineering Research Center of Microbial Metabolism and Fermentation Process Control, College of Biotechnology, Tianjin University of Science & Technology, Tianjin 300457, China.

出版信息

Nutrients. 2018 Jun 22;10(7):805. doi: 10.3390/nu10070805.

Abstract

Shanxi aged vinegar (SAV) is a typical fermented and antioxidant food, which has various health-promoting effects. This work aimed to explore the effects of SAV on alcohol-induced liver injury. A mice model of alcoholic liver injury was established to illuminate its potential mechanisms. All mice pretreated with SAV and then received an ethanol solution (50% /, 4.8 g/kg b.w.). The results showed that SAV ameliorated alcohol-induced histological changes and elevation of liver enzymes. SAV attenuated alcohol-induced oxidative stress by declining levels of hepatic oxidants, and restoring depletion of antioxidant enzyme activities in mice livers. Moreover, SAV alleviated alcohol-induced oxidative damage by activating nuclear factor erythroid-2-related factor 2 (Nrf2)-mediated signal pathway. In addition, SAV prevented alcohol-induced inflammation by suppressing lipopolysaccharide (LPS) level and activities of pro-inflammatory enzymes, and regulating inflammatory cytokines. SAV inhibited alcohol-induced inflammation through down-regulating the expression of Toll-like receptor 4 (TLR4)-mediated inflammatory response. The findings provide crucial evidence for elucidating the hepatoprotective mechanisms of SAV and encourage the future application of SAV as a functional food for liver protection.

摘要

山西老陈醋(SAV)是一种典型的发酵和抗氧化食品,具有多种促进健康的作用。本研究旨在探讨 SAV 对酒精性肝损伤的作用。建立酒精性肝损伤小鼠模型以阐明其潜在机制。所有小鼠用 SAV 预处理,然后给予乙醇溶液(50%/,4.8 g/kg b.w.)。结果表明,SAV 改善了酒精引起的组织学变化和肝酶升高。SAV 通过降低肝氧化剂水平,恢复小鼠肝脏抗氧化酶活性的耗竭,减轻酒精引起的氧化应激。此外,SAV 通过激活核因子红细胞 2 相关因子 2(Nrf2)介导的信号通路,减轻酒精引起的氧化损伤。此外,SAV 通过抑制脂多糖(LPS)水平和促炎酶的活性以及调节炎症细胞因子来预防酒精引起的炎症。SAV 通过下调 Toll 样受体 4(TLR4)介导的炎症反应来抑制酒精引起的炎症。这些发现为阐明 SAV 的保肝机制提供了重要证据,并鼓励未来将 SAV 作为一种具有肝脏保护功能的功能性食品加以应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/864d/6073858/ef6f882bc61d/nutrients-10-00805-g001.jpg

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