BACKGROUND Various extracts of Hovenia dulcis have been commonly used in Asia for cases of alcohol-related disorders. Fermentation is reported to enhance the level and biological activities of various bio-constituents of plant extracts. Therefore, this study was undertaken to evaluate the effects of fermented H. dulcis extract (FHDE) on ethanol-induced liver injury in mice. METHODS FHDE was prepared using Bacillus subtilis and Lactobacillus plantarum. The effects of FHDE on ethanol-induced liver injury were evaluated in C57BL/6 N CrSlc mice. A mixed feed preparation containing the fermented extract with and without ethanol was given to mice for 29 days, according to its group. At the end of the experiment, blood and liver samples were collected from all mice in the group. Plasma biochemical analysis and histopathological investigation were performed to evaluate the impacts of treatment on the biomarkers of hepatic damage and inflammatory changes. Besides, the expression of genes that regulate the activities of enzymes associated with alcohol metabolism, antioxidant activity, and fatty acid oxidation was assessed using a quantitative real-time polymerase chain reaction. Moreover, the amino acid contents and the active ingredients of the extract were evaluated before and after fermentation. RESULTS Fermentation resulted in a marked increase and decrease in the amount of Gamma-Amino-n-butyric acid (GABA) and glutamic acid, respectively. FHDE enhanced the body weight gain of mice compared to ethanol. Besides, plasma levels of triglyceride, low-density lipoprotein, the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were significantly (P < 0.05) reduced in the FHDE-treated groups relative to the ethanol-treated control. FHDE upregulated the expression of genes associated with enzymes involved in alcohol dehydrogenation (Adh1 and Aldh2), antioxidant activity (SOD and CAT), and fatty acid oxidation (PPAR-α and PGC-1α). However, the expressions of Cytochrome peroxidase Cyp2E1 and genes related to lipogenesis (SREBP-1c, FAS, SCD-1, and ACC) were significantly (P < 0.05) downregulated following treatment with the FHDE. Histopathological investigation demonstrated a slight degree of inflammatory cell infiltration and occasional fatty changes in the FHDE-treated groups. CONCLUSION The GABA-enriched fermented H. dulcis extract prevented ethanol-induced hepatic damage by enhancing the antioxidant defense system, fatty acid oxidation, and reducing lipogenesis.

中文翻译：

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富含γ-氨基丁酸的发酵Ho糖提取物对小鼠乙醇诱导的肝损伤的肝保护作用。

背景技术在亚洲，酒精度过高的情况下，人们普遍使用了Hovenia dulcis的各种提取物。据报道，发酵可以提高植物提取物中各种生物成分的水平和生物活性。因此，进行了这项研究，以评估发酵的H. dulcis提取物（FHDE）对乙醇诱导的小鼠肝损伤的影响。方法用枯草芽孢杆菌和植物乳杆菌制备FHDE。在C57BL / 6 N CrSlc小鼠中评估了FHDE对乙醇诱导的肝损伤的影响。根据其组，将含有和不含有乙醇的发酵提取物的混合饲料制剂给予小鼠29天。实验结束时，从该组所有小鼠中采集血液和肝脏样品。进行血浆生化分析和组织病理学研究以评估治疗对肝损害和炎症改变的生物标志物的影响。此外，使用定量实时聚合酶链反应评估调节与酒精代谢，抗氧化活性和脂肪酸氧化有关的酶活性的基因的表达。此外，在发酵之前和之后评估提取物的氨基酸含量和活性成分。结果发酵导致γ-氨基-正丁酸（GABA）和谷氨酸的量分别显着增加和减少。与乙醇相比，FHDE增强了小鼠的体重增加。此外，血浆甘油三酸酯，低密度脂蛋白，与乙醇处理的对照组相比，FHDE处理组的天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）活性显着降低（P <0.05）。FHDE上调了与酒精脱氢酶（Adh1和Aldh2），抗氧化活性（SOD和CAT）和脂肪酸氧化（PPAR-α和PGC-1α）相关的酶相关基因的表达。但是，用FHDE处理后，细胞色素过氧化物酶Cyp2E1的表达和与脂肪生成有关的基因（SREBP-1c，FAS，SCD-1和ACC）显着下调（P <0.05）。组织病理学研究表明，FHDE治疗组的炎症细胞浸润程度较轻，偶尔有脂肪变化。结论富含GABA的发酵H.