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茯砖茶通过调节肠道微生物群-肝脏轴和抑制肝 TLR4/NF-κB 信号通路来缓解酒精性肝损伤。

Fu brick tea alleviates alcoholic liver injury by modulating the gut microbiota-liver axis and inhibiting the hepatic TLR4/NF-κB signaling pathway.

机构信息

Shaanxi Engineering Laboratory for Food Green Processing and Safety Control, and Shaanxi Key Laboratory for Hazard Factors Assessment in Processing and Storage of Agricultural Products, College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an 710119, China.

Key Laboratory of Ministry of Education for Medicinal Resource and Natural Pharmaceutical Chemistry, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.

出版信息

Food Funct. 2022 Sep 22;13(18):9391-9406. doi: 10.1039/d2fo01547a.

DOI:10.1039/d2fo01547a
PMID:35959866
Abstract

This study first evaluated the protective effects of Fu brick tea water extracts (FTE) on alcoholic liver injury and its underlying mechanism in C57BL/6J mice. Oral administration of FTE by oral gavage (400 mg per kg bw) for 12 weeks significantly alleviated lipid metabolism disorder, reduced the activities of serum ALT and AST, decreased the expression of the liver CYP2E1 gene, and enhanced the antioxidant capacities of the livers in alcohol-fed mice ( < 0.05). FTE also relieved alcohol-induced gut microbiota dysbiosis by promoting the proliferation of probiotics such as and , and subsequently increased the cecal levels of short-chain fatty acids (SCFAs) and decreased the tryptophan content of alcohol-fed mice ( < 0.05). Importantly, FTE was found to improve the alcohol-impaired gut barrier function by up-regulating the expression of the epithelial tight junction protein. Accordingly, FTE decreased the circulating lipopolysaccharide (LPS) and thus inhibited the hepatic TLR4/NF-κB signaling pathway to ameliorate alcoholic liver injury. Cumulatively, these findings shed light on the important role of the gut microbiota-liver axis behind the protective efficacy of FTE on alcoholic liver injury.

摘要

本研究首先评估了茯砖茶水提物(FTE)对 C57BL/6J 小鼠酒精性肝损伤的保护作用及其潜在机制。灌胃给予 FTE(400mg/kg bw)12 周可显著缓解脂代谢紊乱,降低血清 ALT 和 AST 活性,下调酒精喂养小鼠肝脏 CYP2E1 基因表达,增强肝脏抗氧化能力(<0.05)。FTE 通过促进 和 等益生菌的增殖缓解酒精诱导的肠道菌群失调,从而增加盲肠短链脂肪酸(SCFAs)水平并降低酒精喂养小鼠的色氨酸含量(<0.05)。重要的是,FTE 通过上调上皮紧密连接蛋白的表达改善了酒精损伤的肠道屏障功能。因此,FTE 降低了循环脂多糖(LPS)水平,从而抑制了肝 TLR4/NF-κB 信号通路,改善了酒精性肝损伤。综上所述,这些发现揭示了肠道微生物群-肝脏轴在 FTE 对酒精性肝损伤保护作用中的重要作用。

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