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The intake of excessive ethanol will activate an alternative ethanol metabolic pathway in the liver, resulting in the overproduction of reactive oxygen species (ROS), which further leads to alcoholic liver injury (ALI). Although several molecular antioxidants have been utilized in clinics for treating ALI, their efficacies are still less satisfactory. In this work, a nanocatalytic antioxidation therapeutic strategy is proposed for ALI treatment by constructing amorphous Co(OH)2 nanosheets with catalytic antioxidative property. The bis(μ‐hydroxo)CoIICoII dinuclear active sites of Co(OH)2 nanosheets are capable of coordinating with hydrogen peroxide (H2O2) with significantly reduced thermodynamic barrier to form a dihydroxyl adduct bis(μ‐hydroxo)CoIII(OH)CoIII(OH) favorable for catalytic H2O2 disproportionation, while amorphous and ultrathin structure further facilitates the reaction, resulting in a high catalytic efficiency (Km=59.31 mM). Thanks to the inherent hepatic passive targeting ability of nanomaterials, the antioxidative nanosheets can accumulate in liver region efficiently after intravenous administration (35.5 % ID/g accumulation efficiency), enabling efficient catalytic antioxidation in the liver to mitigate hepatic oxidative stress, protect hepatocytes from apoptosis/ferroptosis. This study provides a new methodology of nanocatalytic antioxidation for treating ALI and other hepatic diseases related to oxidative stress. [ABSTRACT FROM AUTHOR]

Chimonanthus salicifolius, a traditionally unique medicinal herb in China and Asian countries, is capable of inhibiting pathogenic bacteria; and, hence, has been applied for healthy food. To explore its functional characteristics, the present study analyzed the main components of C. salicifolius polysaccharides (CSP) and examined the hepatoprotective effect of CSP through using an established mouse model of acute alcoholic liver injury. Additionally, the oxidative stress and inflammatory indicators were measured, and the hepatoprotective mechanism of CSP was revealed. The results indicated that the main components in CSP were galactose, glucose, arabinose, and mannose. After administration, CSP significantly decreased the levels of alanine aminotransferase, aspartate aminotransferase, triglyceride, and total cholesterol in alcoholic liver injury mice. CSP could remarkably alleviate liver damage from histopathological examination; increase the antioxidant activity of superoxide dismutase, glutathione, and glutathione peroxidase; decrease the levels of hepatic inflammation of TNF-α, IL-1β, and IL-6; and regulate the NF-κB signaling pathway. These findings demonstrated that CSP effectively improved acute alcoholic liver injury in mice and could be considered as a potential candidate for ALI treatment. [ABSTRACT FROM AUTHOR]

Bacillus subtilis has been reported to maintain the homeostasis of intestinal flora. In this study, a mouse model of alcoholic liver injury (ALI) was constructed to study the ameliorative effect of B. subtilis C10 on ALI and to further clarify its mechanism of action. Significant correlations between intestinal flora and biochemical indicators of ALI were found by statistical correlation analysis. Supplementation with B. subtilis C10 modulated the equilibrium of gut flora by reducing the population of detrimental bacteria while enhancing the numbers of beneficial microorganisms, which resulted in an improvement in lipid metabolism and oxidative stress in the liver. The results of RT‐qPCR showed that B. subtilis C10 intervention regulated the main regulatory factors of liver lipid metabolism (PPAR‐α, SREBP‐1c) and interfered with Nrf‐2/Ho‐1 signal pathway, which in turn ameliorated alcohol‐induced lipid metabolism disorder and liver peroxidation stress. In addition, liver metabonomic analysis showed that B. subtilis C10 intervention reduced the production of harmful metabolites and increased beneficial metabolites in the liver, thereby reversing the metabolic disturbances caused by excessive alcohol consumption. KEGG analysis showed that B. subtilis C10 intervention modulated liver metabolic disorders and accelerated lipid metabolism by regulating glutathione metabolic pathway, purine metabolic pathway, pantothenic acid and CoA biosynthesis pathway, ABC transporter protein pathway, and HIF‐1 signaling pathway. Taken together, these findings suggest that B. subtilis C10 ameliorates ALI by modifying the structure of intestinal flora and liver metabolic pathways to attenuate alcohol‐exposure‐induced liver oxidative damage and lipid metabolism abnormalities. Practical Application: Bacillus subtilis C10 is an effective probiotic intervention that significantly ameliorated alcoholic liver injury in mice through the gut–liver axis. B. subtilis C10 can be used as a dietary probiotic to develop functional foods with beneficial effects for the population of excessive alcohol consumption. [ABSTRACT FROM AUTHOR]

The hepatoprotective effect of the alcoholic extracts of Ganoderma lucidum fermentation products (GFE) was investigated. C57BL/6 mice were pretreated with GFE for 7 days and then subjected to the chronic-binge ethanol feeding model. GFE pretreatment significantly reduced the ethanol-induced elevated serum levels of aspartate aminotransferase (AST) and alanine transaminase (ALT), hepatic steatosis, and increased triglyceride content. GFE pretreatment also altered hepatic alcohol metabolism, suppressed oxidative stress by decreasing the expression of Cyp2e1, and increasing the level of GSH. Lipidmoic analysis revealed that GFE pretreatment effectively increased ratio of phosphatidylcholines /phosphatidylethanolamine (PC/PE) in the liver. Furthermore, mice pretreated with GFE demonstrated decreased hepatic inflammation and plasma lipopolysaccharide (LPS) levels. Additionally, the mRNA expression of gut tight junction proteins such as ZO-1, Occludin and Claudin-1, along with antimicrobial peptide (e.g., Reg3β and Reg3γ) were up-regulated by GFE pretreatment. 16s rRNA sequencing revealed that GFE increased Bacteroidales, Parabacteroides, and Dubosiella, which were associated with hepatic steatosis, inflammation and intestinal barrier function parameters. These results demonstrate that GFE can prevent ethanol-induced liver injury and inflammation, gut leakiness and restore gut microbiota dysbiosis. [ABSTRACT FROM AUTHOR]

Objective: To investigate the antioxidant effect of peptides from Argopecten irradians and its protective effect and mechanism against ethanol-induced alcoholic liver injury in mice. Methods: A. irradians peptides were prepared by two-step enzymatic hydrolysis followed by membrane separation. The in vitro antioxidant activity of A. irradians peptides, the activating effects on superoxide dismutase (SOD) and alcohol dehydrogenase (ADH) and the potential to promote alcohol metabolism were evaluated. The protective effect and mechanism against alcoholic liver injury in mice were investigated by measuring the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the serum, and the activities of ADH, acetaldehyde dehydrogenase (ALDH), glutathione peroxidase (GSH-Px), catalase (CAT) and SOD and malondialdehyde (MDA) content in the liver of a mouse model of acute alcoholism. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to analyze the peptide sequences. PeptideRanker and AnOxPePred 1.0 tools were used to predict the potential biological activity of peptides and conduct molecular docking analysis of the peptide with the strongest antioxidant activity to ALDH. Results: Peptides with molecular mass between 200 and 1 000 Da constituted approximately 70.38% of the total peptides. Antioxidant amino acids accounted for 68.75% of the total amino acids. In vitro experiments showed that the half maximal inhibitory concentration (IC50) values of A. irradians peptides were 19.43, 4.53 and 2.19 mg/mL in 1,1-diphenyl-2-picrylhydrazyl (DPPH) and hydroxyl radical scavenging and Fe2+ chelating assays, respectively. At 5 mg/mL, the hydrolysate of A. irradians activated SOD and ADH by 19.83% and 18.18%, respectively, demonstrating good antioxidant activity and anti-alcoholic potential. In vivo experimental results showed that A. irradians peptides significantly reduced the levels of ALT and AST in mouse serum, enhanced the activity of ADH, ALDH, GSH-Px, SOD and CAT, and reduced the content of MDA. Using PeptideRanker and AnOxPePred 1.0 tools, 44 identified peptides were screened, and 6 of them met the criteria for molecular docking screening. Molecular docking revealed that they had strong binding capacity to ALDH. Among them, DQPHFPF and YSTHPHF formed 7 and 3 hydrogen bonds with ALDH, respectively, which could be activated through molecular interactions with ALDH. Conclusion：This study provides a theoretical reference for the application of peptides products from A. irradians for curing alcohol and protecting liver.

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Fish sperm extracts have been shown to have various activities, but it has not been effectively developed and utilized at present due to the lack of effective methods for preparing edible grade products. This study proposed a method for preparing edible fish sperm DNA from Alaska pollock (PSD) and evaluated the hepatoprotective effect of the extracted DNA. Firstly, the preparation conditions of fish sperm DNA were optimized by response surface methodology. Under the ideal conditions that the ratio of solid to liquid was 3:1, the pH of extractant was 7.5, the purified solvent was saturated sodium carbonate solution and absolute ethanol was twice the volume of purified solvent, the yield of PSD was (13.657 ± 0.577) µg/mg. To evaluate the liver protective effects of the extracted DNA, the digestion products by three digestion enzymes (pepsin, DNase I and DNase II) compared using an alcohol-induced HepG2 cell model. The DNase I hydrolysis product was more effective in preventing cell alcohol damage, as shown by reducing the content of lipid peroxides. Transcriptomics and metabolomics data revealed that the DNase I hydrolysis product activated the Nrf2/HO-1 pathway through the PI3K/Akt signaling pathway and regulated abnormal lipid synthesis through the steroidogenic pathway. This study will provide an important basis for the evaluation and analysis of the hepatoprotective effect of fish sperm DNA in vivo. Overall, our findings will promote the comprehensive utilization of fish sperm and other aquatic wastes, and provide scientific guidance for the development of functional nucleic acid foods. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Alcoholic liver disease (ALD) is regarded as one of the main global health problems. Accumulated evidence indicates that fruit-derived polyphenols can lower the risk of ALD, this attributed to their strong antioxidant capacities. Thinned immature kiwifruits (TIK) are the major agro-byproducts in the production of kiwifruits, which have abundantly valuable polyphenols. However, knowledge about the protective effects of polyphenol-enriched extract from TIK against ALD is still lacking, which ultimately restricts their application as value-added functional products. To promote their potential applications, phenolic compounds from TIK and their corresponding mature fruits were compared, and their protective effects against ALD were studied in the present study. The findings revealed that TIK possessed extremely high levels of total phenolics (116.39 ± 1.51 mg GAE/g DW) and total flavonoids (33.88 ± 0.59 mg RE/g DW), which were about 7.4 times and 4.8 times greater than those of their corresponding mature fruits, respectively. Furthermore, the level of major phenolic components in TIK was measured to be 29,558.19 ± 1170.58 μg/g DW, which was about 5.4 times greater than that of mature fruits. In particular, neochlorogenic acid, epicatechin, procyanidin B1, and procyanidin B2 were found as the predominant polyphenols in TIK. In addition, TIK exerted stronger in vitro antioxidant and anti-inflammatory effects than those of mature fruits, which was probably because of their higher levels of polyphenols. Most importantly, compared with mature fruits, TIK exhibited superior hepatoprotective effects on alcohol-induced liver damage in mice. The administration of polyphenol-enriched extract from TIK (YK) could increase the body weight of mice, reduce the serum levels of ALP, AST, and ALT, lower the levels of hepatic TG and TC, and diminish lipid droplet accumulation and hepatic tissue damage. In addition, the treatment of YK could also significantly restore the levels of antioxidant enzymes (e.g., SOD and CAT) in the liver and lower the levels of hepatic proinflammatory cytokines (e.g., IL-6, IL-1β, and TNF-α), indicating that YK could effectively ameliorate ALD in mice by reducing hepatic oxidative stress and hepatic inflammation. Collectively, our findings can provide sufficient evidence for the development of TIK and their extracts as high value-added functional products for the intervention of ALD. [ABSTRACT FROM AUTHOR]

Alcoholic liver disease (ALD) is a globally prevalent form of liver disease for which there is no effective treatment. Recent studies have found that a significant decrease in butyrate was closely associated with ALD development. Given the low compliance and delivery efficiency associated with oral-route butyrate administration, a highly effective butyrate-yielding dietary supplement, butyrylated high-amylose maize starch (HAMSB), is a good alternative approach. Here, we synthesized HAMSB, evaluated the effect of HAMSB on acute ALD in mice, compared its effect with that of oral administration of butyrate, and further studied the potential mechanism of action. The results showed HAMSB alleviated acute ALD in mice, as evidenced by the inhibition of hepatic-function impairment and the improvement in liver steatosis and lipid metabolism; in these respects, HAMSB supplementation was superior to oral sodium butyrate administration. These improvements can be attributed to the reduction of oxidative stress though the regulation of Nrf2-mediated antioxidant signaling in the liver and the improvement in the composition and function of microbiota in the intestine. In conclusion, HAMSB is a safe and effective dietary supplement for preventing acute ALD that could be useful as a disease-modifying functional food or candidate medicine. [ABSTRACT FROM AUTHOR]

Annulohypoxylon stygium melanin (AsM) has various functional properties such as antioxidant and anti-radiation, but its biological activity in vivo has not been fully investigated. In this study, we researched the effects of AsM on the protection against acute liver injury in mice and its mechanism. The results showed that AsM had no significant effect on body weight in mice but reduced the liver index. It was able to significantly decrease the activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT), the contents of triglyceride (TG) and total cholesterol (TC) in mice. Simultaneously, it raised the levels of superoxide dismutase (SOD), peroxidase (CAT), and glutathione peroxidase (GSH-Px), which obviously exceeded those of the EtOH group. AsM could significantly lower the levels of inflammatory factors, with inhibition rates of 68.30%, 29.0%, and 19.50% for IL-1β, IL-6, and TNF-α, respectively. H&E and Oil red O staining also showed that AsM ameliorated liver damage and lipid accumulation in mice. The protective mechanism of AsM may be associated to the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant signaling pathway, which could activate the downstream antioxidant enzymes heme oxygenase-1 (HO-1), glutamate-cysteine ligase modifier subunit (GCLM), and glutamate-cysteine ligase catalytic subunit (GCLC). These findings confirmed that AsM had an alleviating effect on alcoholic liver injury and provided new thoughts for the development of natural product. [ABSTRACT FROM AUTHOR]

Ganoderma lucidum, used in East Asia for its health benefits, contains ganoderic acids (GA) which have various pharmacological activities but are limited by poor water solubility and low oral bioaccessibility. This study synthesized and characterized ganoderic acids loaded zein-chitosan nanoparticles (GA-NPs), and investigated its advantages in alleviating alcoholic liver injury (ALI) in mice model. The GA-NPs demonstrated high encapsulation efficiency (92.68%), small particle size (177.20 nm), and a +29.53 mV zeta potential. The experimental results of alcohol-induced liver injury mouse model showed that GA-NPs significantly improved liver metabolic function, reduced alcohol-induced liver oxidative stress in liver by decreasing lactate dehydrogenase activity and malondialdehyde level, while increasing the activities of liver antioxidant enzymes and alcohol dehydrogenase. Moreover, GA-NPs were favorable to ameliorate intestinal microbiota dysbiosis in mice exposed to alcohol by increasing the proportion of probiotics such as Romboutsia, Faecalibaculum, Bifidobacterium and Turicibacter, etc., which were highly correlated with the improvement of liver function. Furthermore, GA-NPs modulated the mRNA expression related to ethanol metabolism, oxidative stress and lipid metabolism. Conclusively, this study revealed that GA-NPs have stronger hepatoprotective effects than non-encapsulated ganoderic acids on alleviating ALI by regulating intestinal microbiota and liver metabolism. [ABSTRACT FROM AUTHOR]

Liver injury induced by alcohol is a serious global health problem. Several tea-like plants are widely used as beverages, which are drunk like tea. In this study, the hepatoprotective effects of eight tea-like plant extracts with the intake of 200 mg/kg.bw/day were investigated and compared using a C57BL/6J mouse model of acute alcohol exposure, including sweet tea, vine tea, Rabdosia serra kudo, broadleaf holly leaf, mulberry leaf, bamboo leaf, Camellia nitidissima, and Akebia trifoliata peels. The results showed that the eight tea-like plants had hepatoprotective effects to different degrees against acute alcohol exposure via enhancing the activities of alcoholic metabolism enzymes, ameliorating oxidative stress and inflammation in the liver, as well as regulating gut microbiota. In particular, sweet tea, bamboo leaf, mulberry leaf, and Camellia nitidissima increased the activities of alcohol dehydrogenase or aldehyde dehydrogenase. Among these tea-like plants, sweet tea and Camellia nitidissima had the greatest hepatoprotective effects, and their bioactive compounds were determined by high-performance liquid chromatography. Chlorogenic acid, rutin, and ellagic acid were identified in sweet tea, and epicatechin, rutin, and ellagic acid were identified in Camellia nitidissima, which could contribute to their hepatoprotective action. These tea-like plants could be drunk or developed into functional food against alcoholic liver injury, especially sweet tea and Camellia nitidissima. In the future, the effects of sweet tea and Camellia nitidissima on chronic alcoholic liver diseases should be further investigated. [ABSTRACT FROM AUTHOR]

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Selenium-enriched probiotics have attracted much attention due to the physiological activities of both probiotics and selenium (organic selenium). In this study, we investigated the mitigating effect of selenium-enriched Lactobacillus rhamnosus GG (LGG@Se) and its pathway on alcohol-induced liver injury (ALI) in mice. The results showed that LGG@Se was superior to LGG and sodium selenite in alleviating ALI. Oral LGG@Se effectively prevented lipid metabolism disorders and liver oxidative damage in mice caused by excessive alcohol intake. 16S amplicon sequencing showed that LGG@Se intervention increased the abundance of beneficial bacteria and suppressed the growth of harmful bacteria in the intestinal tract of over-drinking mice, and thus effectively modulated the homeostasis of intestinal flora, which were highly correlated with the improvement of liver function. Liver metabolomics analysis indicated that LGG@Se intervention altered liver metabolic profiling, and the characteristic biomarkers were mainly involved in amino acid metabolism, including alanine, aspartate and glutamate metabolism, arginine biosynthesis, etc. In addition, LGG@Se intervention modulated the expression of genes and proteins related to lipid metabolism and oxidative stress in liver of over-drinking mice. Western blot analysis revealed that LGG@Se intervention up-regulated the expression of intestinal barrier function-related proteins, thereby ameliorating alcohol-induced intestinal barrier damage. Collectively, these findings provide scientific evidence that LGG@Se possesses the biological activity of improving alcohol-induced lipid metabolism and intestinal microbiota disorder.

In this study, we devoted attention to the hepatoprotective functions of high Fischer ratio oligopeptides (HFOPs) from Antarctic krill (HFOPs-AK) on alcoholic liver injury of mice. The results indicated that HFOPs-AK significantly improved the pathological state of mice liver and kidney, reduced alanine aminotransferase (ALT) and aspartate transaminase (AST) activities, regulated lipid metabolism, and alleviated the burden on the liver. In addition, HFOPs-AK depicted anti-inflammatory and antioxidant effects by reducing tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) contents and increasing superoxide dismutase (SOD) and catalase (CAT) activities to reduce malondialdehyde (MDA) level. The hepatoprotective mechanism of HFOPs-AK was further revealed by quantitative reverse transcription PCR (RT-qPCR) analysis, and the results proved that HFOPs-AK had the ability to stimulate the adenosine 5‘-monophosphate-activated protein kinase (AMPK)/nuclearrespiratoty factor 2 (Nrf2)/inhibitor of NF-κB (IκBα) signaling pathways, thereby regulating the expression levels of downstream factors. The activation of these signaling pathways is essential for the regulation of lipid metabolism as well as anti-inflammatory and antioxidant functions. This finding offers a novel approach for the development of innovative hepatoprotective agents utilizing HFOPs-AK.

Objective: To predict the mechanism of sea buckthorn in the treatment of alcoholic liver injury based on network pharmacology, and to verify the efficacy of sea buckthorn in the treatment of alcoholic liver injury by establishing an animal model of alcoholic liver injury in zebrafish. Methods: Through the traditional chinese medicine systems pharmacology (TCMSP) and Uniprot database, the effective components and their targets were collected. Venny2.1 was used to find the intersection targets. GeneCards and OMIM databases were used to collect and screen disease targets. STRING v12.0 database was used for PPI network analysis. PDB and PubChem were used to confirm protein structure and small molecular structure. The correlation network of sea buckthorn in the treatment of alcoholic liver injury was constructed by Cytoscape (Version 3.9.1) software network diagram. Gene ontology (GO) and Kyoto encyclopedia of genes (KEGG) database pathway enrichment analysis were performed on the common targets using the Metascape database. Functional verification was performed by zebrafish experiments: Wild-type AB strain zebrafish 3 days after fertilization (3 dpf) were selected. The normal group was fed with normal feeding water, and the other groups were fed in 2% anhydrous ethanol solution to establish an alcoholic liver injury model. Results: After screening, 33 active components of sea buckthorn were obtained, mainly including quercetin, sunflower, catechin and so on. There were 1434 potential targets for the treatment of alcoholic liver injury, including ADH1C, CTNNB1, TGFB1 and so on. The signaling pathways that regulate these core targets are mainly enriched in multiple signaling pathways such as lipid and atherosclerosis, fluid shear stress and atherosclerosis and PI3K-Akt signaling pathway. The results of animal experiments showed that sea buckthorn had the effect of reducing the opacity value of zebrafish liver in alcoholic liver injury model (P

Objective To evaluate the antioxidant effect of American ginseng Rhodiola formula on ethanol-induced oxidative damage in model mice, and to explore its mechanism of action, providing a scientific basis for the development of healthy food. Methods Mice were randomly divided into blank control group, acute oxidative injury model group, low dose (330 mg/kg), medium dose (660 mg/kg) and high dose (990 mg/kg) groups according to body weight, 10 mice in each group. Each dose group was given test samples by oral gavage. Blank control group and model group were given equal volume of distilled water. After continuous gavage for 30 days, 50% ethanol was intragastrically administered at 12 mL/kg after fasting for 16 h in each group except blank control group. Blood and liver were collected from mice 6 h later. Malondialdehyde (MDA), 8-epoxyisoprostane (8-Isoprostane), protein carbonyl (PCO), glutathione (GSH), aspartate aminotransferase (AST), alanine aminotransferase (ALT), triglyceride (TG), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin- 6 (IL- 6) content and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activity in mouse serum, MDA, PCO, GSH content and SOD activity in liver tissue were measured, and the protein expression of p-p38, p-ERK and p-JNK was detected by Western blotting.. Results Compared with the model group, the MDA content in the serum of mice in the low-dose group of American ginseng Rhodiola formula decreased (P

Abstract Octacosanol is a plant natural product with the potential to ameliorate alcoholic liver injury. However, its poor solubility limits its application in the food industry. This study first verified that octacosanol has a favorable effect on acute and subchronic alcoholic liver injury in mice by protecting the gastric mucosa and ameliorating disease levels. Additionally, octacosanol microcapsules were prepared under the optimal drying conditions of the feed flow rate of 400 mL/h and drying temperature of 180°C to improve the ameliorative effects of octacosanol, with moisture content, water activity, dispersibility, and solubility of 1.53%, 0.16%, 89.84%, and 95.30%, respectively. The microcapsules had a spherical structure, and the droplet sizes after redissolution ranged from 0.061 to 4.63 µm. Instrumental measurements and simulated digestion experiments have shown that microencapsulation enhanced the solubility and thermal stability of octacosanol, with 90.88% of the octacosanol being continuously released. As expected, microencapsulation significantly enhanced the effect of octacosanol in ameliorating alcoholic liver injury by determining the disease index in the mice model. This study demonstrated the beneficial effects of octacosanol on alcoholic liver injury and explored a viable method to improve its solubility and bioaccessibility, thereby enhancing its therapeutic efficacy for the treatment of alcoholic liver injury.

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Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Octacosanol is a plant natural product with the potential to ameliorate alcoholic liver injury. However, its poor solubility limits its application in the food industry. This study first verified that octacosanol has a favorable effect on acute and subchronic alcoholic liver injury in mice by protecting the gastric mucosa and ameliorating disease levels. Additionally, octacosanol microcapsules were prepared under the optimal drying conditions of the feed flow rate of 400 mL/h and drying temperature of 180°C to improve the ameliorative effects of octacosanol, with moisture content, water activity, dispersibility, and solubility of 1.53%, 0.16%, 89.84%, and 95.30%, respectively. The microcapsules had a spherical structure, and the droplet sizes after redissolution ranged from 0.061 to 4.63 µm. Instrumental measurements and simulated digestion experiments have shown that microencapsulation enhanced the solubility and thermal stability of octacosanol, with 90.88% of the octacosanol being continuously released. As expected, microencapsulation significantly enhanced the effect of octacosanol in ameliorating alcoholic liver injury by determining the disease index in the mice model. This study demonstrated the beneficial effects of octacosanol on alcoholic liver injury and explored a viable method to improve its solubility and bioaccessibility, thereby enhancing its therapeutic efficacy for the treatment of alcoholic liver injury. [ABSTRACT FROM AUTHOR]

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Background & aims: Extracellular nicotinamide phosphoribosyltransferase (eNAMPT) has long been recognized as an adipokine. However, the exact role of eNAMPT in alcoholic liver disease (ALD) and its relevance to brown adipose tissue (BAT) remain largely unknown. This study aimed to evaluate the impact of eNAMPT on liver function and the underlying mechanisms involved in BAT-Liver communication. Methods: Serum eNAMPT levels were detected in the serum of both ALD patients and mice. Chronic and binge ethanol feeding was used to induce alcoholic liver injury in mice. An eNAMPT antibody, a coculture model of brown adipocytes and hepatocytes, and BAT-specific Nampt knockdown mice were used to investigate the role of eNAMPT in ALD. Results: Serum eNAMPT levels are elevated in ALD patients and are significantly positively correlated with the liver injury index. In ALD mice, neutralizing eNAMPT reduced the elevated levels of circulating eNAMPT induced by ethanol and attenuated liver injury. In vitro experiments revealed that eNAMPT induced hepatocyte ferroptosis through the TLR4-dependent mitochondrial ROS-induced ferritinophagy pathway. Furthermore, ethanol stimulated eNAMPT secretion from brown adipocytes but not from other adipocytes. In the coculture model, ethanol-induced release of eNAMPT from brown adipocytes promoted hepatocyte ferroptosis. In BAT-specific Nampt-knockdown mice, ethanol-induced eNAMPT secretion was significantly reduced, and alcoholic liver injury were attenuated. These effects can be reversed by intraperitoneal injection of eNAMPT. Conclusion: Inhibition of ethanol-induced eNAMPT secretion from BAT attenuates liver injury and ferroptosis. Our study reveals a previously uncharacterized critical role of eNAMPT-mediated BAT-Liver communication in ALD and highlights its potential as a therapeutic target.

Objective: To explore the preventive effect of Lactobacillus paracasei FZU103 (LP-FZU103) on alcoholic liver injury (ALI). Methods: Altogether 36 specific pathogen free- (SPF-) grade ICR mice were randomly divided into three groups: control, model and experimental (LP-FZU103 intervention). After the six-week experiment, body mass, organ coefficients, serum and liver biochemical indexes, liver histopathology and inflammatory cytokines, the transcription of liver function-related genes and intestinal flora composition were measured. Results: Compared with the model group, intervention of LP-FZU103 improved the organ coefficients and pathological liver damage in ALI mice, significantly reduced the levels of total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) as well as the activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the serum, increased the serum concentration of high-density lipoprotein cholesterol (HDL-C), significantly increased the activity of catalase (CAT) and superoxide dismutase (SOD) and the content of glutathione (GSH) in the liver, and decreased MDA content and interleukin-6 (IL-6), interferon-γ (IFN-γ) levels in the liver. Moreover, LP-FZU103 intervention significantly up-regulated the mRNA expression level of the lipid metabolism-related gene Ldlr and down-regulated the mRNA expression level of Acc1, Hmgcr and Cd36 as well as increased the relative abundance of beneficial bacteria such as Lactobacillus johnsonii, Lactobacillus reuteri and Lactobacillus paracasei in the gut of mice. Conclusion: LP-FZU103 intervention can prevent and control the occurrence of alcoholic liver injury in mice, which is closely related to the improved intestinal flora and liver metabolic function.

Objective: In this work, the optimal preparation process parameters of selenium-curcumin nanoparticles (SeNPs@Cur) were explored and its protective effect on alcoholic liver injury was evaluated. Methods: On the basis of single factor experiment, with particle size as the index, curcumin dosage, molar ratio of VC to Na2SeO3, reaction time and reaction temperature were selected as influence factors. The process parameters of SeNPs@Cur were optimized by response surface methodology, and its structure was characterized by scanning electron microscope (SEM), fourier transform infrared spectrometer (FT-IR) and energy dispersive spectrometer (EDS). The protective effect of SeNPs@Cur on ethanol-induced LO2 cell injury was investigated by MTT method. Results: The optimal conditions of SeNPs@Cur were list as follows: Curcumin dosage of 5.92 mg/mL, molar ratio of VC to Na2SeO3 of 10.39:1, the reaction time of 1.98 h, and the reaction temperature of 34.00 ℃. Under these conditions, the SeNPs@Cur with a minimum size of (100.79±3.46) nm was obtained. The loading rate of curcumin and the selenium content in the sample were 12.80%±0.80% and 23.32%±0.07%, respectively. Further structural identification showed that the prepared SeNPs@Cur was dispersed spherical nanoparticles. Moreover, compared with the model group, after treatments with different dosages of SeNPs@Cur, the cell viabilities increased from 58.06%±0.43% to 71.43%±1.39%, 77.33%±3.54%, and 85.41%±4.61%, respectively, indicating that SeNPs@Cur had a protective effect on LO2 cells damaged by ethanol in a concentration-dependent manner. Conclusion: The SeNPs@Cur with anti-alcoholic liver injury effect was successfully obtained, which provided new technical means and theoretical reference data for formulation improvement and application of curcumin.

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Alcoholic liver injury is a serious risk to human health. Probiotics have become a popular form of treatment. Lacticaseibacillus casei Grx12 and Limosilactobacillus fermentum Grx07 isolated from the gut of long-lived people in Rugao, Jiangsu, were studied to determine their protective effects and possible mechanisms of action on alcoholic liver injury. The results showed that rat serum ALT and AST were restored, and liver injury was reduced after the probiotics intervention. The level of antioxidant enzymes and antioxidants such as SOD, GSH and GSH-Px in the rat liver was significantly increased (p < 0.05), which reduces the level of MDA, a peroxidation product in the liver, and thus alleviates liver oxidative stress. L. casei Grx12 and L. fermentum Grx07 also could significantly enhance the expression of Nrf2 protein in the rat liver to regulate the anti-oxidative stress response in the body and cells (p < 0.05). The levels of ADH, Na+ -K+ -ATPase and Ca2+-ATPase in the rat liver were significantly increased (p < 0.05), which enhanced the body’s metabolism of alcohol. The rat serum LPS and liver TNF-α, IL-6, VEGF, TGF-β1 and NF-κB levels were significantly reduced (p < 0.05), indicating that the probiotics could relieve liver inflammation. The results of this study indicate that L. casei Grx12 and L. fermentum Grx07 have certain protective effects on alcoholic liver injury in rats, likely because of their antioxidant properties and ability to prevent oxidative stress and relieve inflammation. [ABSTRACT FROM AUTHOR]

Alcoholic liver disease (ALD) is primarily caused by long-term excessive alcohol consumption. Cyanidin-3-O-glucoside (C3G) is a widely occurring natural anthocyanin with multiple biological activities. This study aims to investigate the effects of C3G isolated from black rice on ALD and explore the potential mechanism. C57BL/6J mice (male) were fed with standard diet (CON) and Lieber-DeCarli liquid-fed (Eth) or supplemented with a 100 mg/kg/d C3G Diet (Eth-C3G), respectively. Our results showed that C3G could effectively ameliorate the pathological structure and liver function, and also inhibited the accumulation of liver lipids. C3G supplementation could partially alleviate the injury of intestinal barrier in the alcohol-induced mice. C3G supplementation could increase the abundance of Norank_f_Muribaculaceae, meanwhile, the abundances of Bacteroides, Blautia, Collinsella, Escherichia-Shigella, Enterococcus, Prevotella, [Ruminococcus]_gnavus_group, Methylobacterium-Methylorubrum, Romboutsia, Streptococcus, Bilophila, were decreased. Spearman's correlation analysis showed that 12 distinct genera were correlated with blood lipid levels. Non-targeted metabolic analyses of cecal contents showed that C3G supplementation could affect the composition of intestinal metabolites, particularly bile acids. In conclusion, C3G can attenuate alcohol-induced liver injury by modulating the gut microbiota and metabolites, suggesting its potential as a functional food ingredient against alcoholic liver disease. [ABSTRACT FROM AUTHOR]

Rhamnus utilis Decne. (Family Rhamnaceae Juss.) leaf is commonly prepared as a anti-inflammatory herbal medicine and used for tea production. To investigate the mechanism of Rhamnus utilis Decne. aqueous extract (RDAE) against acute alcoholic liver disease (ALD) in mice. The ALD mouse (Male ICR) model was induced via intragastric administration of 52 % alcohol. Mice in each group were treated by gavage once daily with the RDAE (1.12, 2.25, 4.500 g/kg). The expression of proteins involved in the MAPKs/NF-κB/COX-2-iNOS pathway was measured by western blotting. Non-targeted metabolomics was used to determine metabolic profiles and critical pathways, while targeted metabolomics validated key amino acid metabolites. After administration of RDAE, the body mass of mice was significantly increased. The liver index was significantly decreased. Meanwhile, the serum levels of AST, ALT, TG, TC, MDA, TNF-α, IL-1β and IL-6 were significantly decreased (P

Tingxuan Huang, Youjia Wu, Lingyi Huang, Renyi Lin, Zhenyue Li, Xiaoxiao Wang, Pingping Wu, Liying Huang School of Pharmacy, Fujian Medical University, Fuzhou, Fujian, People’s Republic of ChinaCorrespondence: Liying Huang; Pingping Wu, School of Pharmacy, Fujian Medical University, Xuefu North Road University Town, Fuzhou, Fujian, 350122, People’s Republic of China, Tel +8613860635139 ; +8615980271679, Fax +86059422862016, Email fjmuhly88@sina.com; 631763708@qq.comPurpose: Compound Anoectochilus roxburghii (Wall.) Lindl oral liquid (CAROL) is often as a hepatoprotective agent. The present study aimed to elucidate the protective mechanism of CAROL against alcoholic liver injury in rats by untargeted metabolomics combined with multivariate statistical analysis.Methods: An alcoholic liver disease model was established in sprague-dawley (SD) rats by gavage of alcohol, and CAROL treatment was administered. The hepatoprotective effect of CAROL was evaluated by examining liver tissues changes and detecting biochemical index activities and cytokines in serum and liver homogenates. The metabolites in serum samples were examined using ultrahigh-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UHPLC–QTOF/MS) and multivariate statistical analysis to screen for differentially expressed metabolites and Kyoto Encyclopedia of Genes and Genomes (KEGG) to assess potential metabolic pathways.Results: CAROL has the potential to downregulate inflammation levels and alleviate oxidative stress. The differential metabolites are mainly engaged in riboflavin metabolism, arginine and proline metabolism, phenylalanine, tyrosine and tryptophan biosynthesis metabolism, phenylalanine metabolism, pyrimidine metabolism, and vitamin B6 metabolism to achieve hepatoprotective effects.Conclusion: CAROL may exhibit beneficial hepatoprotective effects by reducing inflammation, mitigating oxidative stress, and modulating metabolites and their metabolic pathways.This study has important implications for advancing the clinical application of CAROL. Keywords: compound Anoectochilus roxburghii (Wall.) Lindl. oral liquid, alcoholic liver injury, untargeted metabolomics, UHPLC–QTOF/MS, metabolic pathway analysis

Alcoholic liver disease (ALD) is regarded as one of the main global health problems. Accumulated evidence indicates that fruit-derived polyphenols can lower the risk of ALD, this attributed to their strong antioxidant capacities. Thinned immature kiwifruits (TIK) are the major agro-byproducts in the production of kiwifruits, which have abundantly valuable polyphenols. However, knowledge about the protective effects of polyphenol-enriched extract from TIK against ALD is still lacking, which ultimately restricts their application as value-added functional products. To promote their potential applications, phenolic compounds from TIK and their corresponding mature fruits were compared, and their protective effects against ALD were studied in the present study. The findings revealed that TIK possessed extremely high levels of total phenolics (116.39 ± 1.51 mg GAE/g DW) and total flavonoids (33.88 ± 0.59 mg RE/g DW), which were about 7.4 times and 4.8 times greater than those of their corresponding mature fruits, respectively. Furthermore, the level of major phenolic components in TIK was measured to be 29,558.19 ± 1170.58 μg/g DW, which was about 5.4 times greater than that of mature fruits. In particular, neochlorogenic acid, epicatechin, procyanidin B1, and procyanidin B2 were found as the predominant polyphenols in TIK. In addition, TIK exerted stronger in vitro antioxidant and anti-inflammatory effects than those of mature fruits, which was probably because of their higher levels of polyphenols. Most importantly, compared with mature fruits, TIK exhibited superior hepatoprotective effects on alcohol-induced liver damage in mice. The administration of polyphenol-enriched extract from TIK (YK) could increase the body weight of mice, reduce the serum levels of ALP, AST, and ALT, lower the levels of hepatic TG and TC, and diminish lipid droplet accumulation and hepatic tissue damage. In addition, the treatment of YK could also significantly restore the levels of antioxidant enzymes (e.g., SOD and CAT) in the liver and lower the levels of hepatic proinflammatory cytokines (e.g., IL-6, IL-1β, and TNF-α), indicating that YK could effectively ameliorate ALD in mice by reducing hepatic oxidative stress and hepatic inflammation. Collectively, our findings can provide sufficient evidence for the development of TIK and their extracts as high value-added functional products for the intervention of ALD.

Liver injury induced by alcohol is a serious global health problem. Several tea-like plants are widely used as beverages, which are drunk like tea. In this study, the hepatoprotective effects of eight tea-like plant extracts with the intake of 200 mg/kg.bw/day were investigated and compared using a C57BL/6J mouse model of acute alcohol exposure, including sweet tea, vine tea, Rabdosia serra kudo, broadleaf holly leaf, mulberry leaf, bamboo leaf, Camellia nitidissima, and Akebia trifoliata peels. The results showed that the eight tea-like plants had hepatoprotective effects to different degrees against acute alcohol exposure via enhancing the activities of alcoholic metabolism enzymes, ameliorating oxidative stress and inflammation in the liver, as well as regulating gut microbiota. In particular, sweet tea, bamboo leaf, mulberry leaf, and Camellia nitidissima increased the activities of alcohol dehydrogenase or aldehyde dehydrogenase. Among these tea-like plants, sweet tea and Camellia nitidissima had the greatest hepatoprotective effects, and their bioactive compounds were determined by high-performance liquid chromatography. Chlorogenic acid, rutin, and ellagic acid were identified in sweet tea, and epicatechin, rutin, and ellagic acid were identified in Camellia nitidissima, which could contribute to their hepatoprotective action. These tea-like plants could be drunk or developed into functional food against alcoholic liver injury, especially sweet tea and Camellia nitidissima. In the future, the effects of sweet tea and Camellia nitidissima on chronic alcoholic liver diseases should be further investigated.

Ganoderma lucidum, used in East Asia for its health benefits, contains ganoderic acids (GA) which have various pharmacological activities but are limited by poor water solubility and low oral bioaccessibility. This study synthesized and characterized ganoderic acids loaded zein-chitosan nanoparticles (GA-NPs), and investigated its advantages in alleviating alcoholic liver injury (ALI) in mice model. The GA-NPs demonstrated high encapsulation efficiency (92.68%), small particle size (177.20 nm), and a +29.53 mV zeta potential. The experimental results of alcohol-induced liver injury mouse model showed that GA-NPs significantly improved liver metabolic function, reduced alcohol-induced liver oxidative stress in liver by decreasing lactate dehydrogenase activity and malondialdehyde level, while increasing the activities of liver antioxidant enzymes and alcohol dehydrogenase. Moreover, GA-NPs were favorable to ameliorate intestinal microbiota dysbiosis in mice exposed to alcohol by increasing the proportion of probiotics such as Romboutsia, Faecalibaculum, Bifidobacterium and Turicibacter, etc., which were highly correlated with the improvement of liver function. Furthermore, GA-NPs modulated the mRNA expression related to ethanol metabolism, oxidative stress and lipid metabolism. Conclusively, this study revealed that GA-NPs have stronger hepatoprotective effects than non-encapsulated ganoderic acids on alleviating ALI by regulating intestinal microbiota and liver metabolism.

Abstract In this study, the hepatoprotective effect of alkali extract (NE) of water bamboo shoot (WBS) against acute alcoholic liver injury (ALI) in mice was evaluated, and its underlying mechanisms were explored. Animal experiment demonstrated that NE exhibited hepatoprotective effect on alcoholic intake‐induced ALI via significantly enhancing the hepatic activities of alcohol dehydrogenase (ADH), acetaldehyde dehydrogenase (ALDH), superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and catalase (CAT), whereas significantly attenuated hepatic levels of malondialdehyde (MDA), interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α). The potential molecular mechanism and bioactive compounds of NE against ALI were explored by bioinformatics analysis and isosinensetin was found to be the major bioactive compounds in NE against ALI. The western blot analysis showed that NE inhibited phosphorylation of p65 and IκBα to suppress the NF‐κB pathway. Overall our result indicated that WBS possesses potential hepatoprotective effects against ALI.

Dianhong Black Tea, a fermented tea containing various bioactive ingredients, has been found to have a significant role in alleviating alcoholic liver injury (ALI). One of its main unique components, Dianhong Black Tea volatile substances (DBTVS), may have potential anti‐ALI effects. However, its effects and underlying molecular mechanisms are still unknown. In this study, we aimed to investigate the potential of DBTVS as an anti‐ALI agent using alcohol‐fed rats. We assessed the effect of DBTVS on ALI by analyzing serum transaminase and lipid levels, as well as conducting hematoxylin–eosin and oil red O staining. Additionally, GC‐MS was used to detect the components of DBTVS, while transcriptome, proteomics analysis, Western blot, and molecular docking were employed to uncover the underlying mechanisms. Our results demonstrated that DBTVS significantly reduced serum ALT and AST levels and improved lipid metabolism disorders. Moreover, we identified 14 components in DBTVS, with five of them exhibiting strong binding affinity with key proteins. These findings suggested that DBTVS could be a promising agent for the prevention and treatment of ALI. Its potential therapeutic effects may be attributed to its ability to regulate lipid metabolism through the PPAR signaling pathway. [ABSTRACT FROM AUTHOR]

Alcohol use accounts for a large variety of diseases, among which alcoholic liver injury (ALI) poses a serious threat to human health. In order to overcome the limitations of chemotherapeutic agents, some natural constituents, especially polysaccharides from edible medicinal plants (PEMPs), have been applied for the prevention and treatment of ALI. In this review, the protective effects of PEMPs on acute, subacute, subchronic, and chronic ALI are summarized. The pathogenesis of alcoholic liver injury is analyzed. The structure–activity relationship (SAR) and safety of PEMPs are discussed. In addition, the mechanism underlying the hepatoprotective activity of polysaccharides from edible medicinal plants is explored. PEMPs with hepatoprotective activities mainly belong to the families Orchidaceae, Solanaceae, and Liliaceae. The possible mechanisms of PEMPs include activating enzymes related to alcohol metabolism, attenuating damage from oxidative stress, regulating cytokines, inhibiting the apoptosis of hepatocytes, improving mitochondrial function, and regulating the gut microbiota. Strategies for further research into the practical application of PEMPs for ALI are proposed. Future studies on the mechanism of action of PEMPs will need to focus more on the utilization of multi-omics approaches, such as proteomics, epigenomics, and lipidomics. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

A large number of data show that the prevalence rate of alcoholic liver injury (ALI) is increasing year by year, and it has become one of the main causes of death due to chronic liver diseases such as liver cancer and liver cirrhosis. Quitting drinking is the main method for the prevention of ALI in modern medicine, and the main treatment methods include Western medicine with antioxidant and anti－fibrotic effects and nutritional support. However, Western medicine tends to have an unsatisfactory treatment effect and can only alleviate initial symptoms, and severe ALI still requires surgical treatment. Studies have shown that the monomers extracted from natural drugs and foods have obvious preventive and therapeutic effects on ALI, with high safety and easy access. Therefore, this article systematically summarizes the main natural drug and food monomers used for the prevention and treatment of ALI and proposes the idea of the combination of drug and food for the prevention and treatment of ALI from the perspective of paying attention to the whole process of health, in order to explore more effective prevention, health care, and treatment methods and provide ideas for research on the prevention and control of ALI. [ABSTRACT FROM AUTHOR]

As alcohol consumption increases, alcoholic liver disease (ALD) has become more popular and is threating our human life. In this study, we found mulberry fruit extract (MFE) repaired alcohol-caused liver diseases by regulating hepatic lipid biosynthesis pathway and oxidative singling in alcoholically liver injured (ALI) rats. MFE administration inhibited hepatic lipid accumulation and improved liver steatosis in ALI rats. MFE also enhanced the antioxidant capacity and alleviated the inflammatory response by increasing the activities of antioxidant enzymes and decreasing the contents of interleukin (IL)-1β and tumor necrosis factor (TNF)-α. Additionally, MFE regulated the expression of miRNA-155 and lipid metabolism–related PPARα protein in rats. Both miR-155 and PPARα play important roles in liver function. The results indicate that MFE has hepatoprotective effects against ALI in rats. [ABSTRACT FROM AUTHOR]

背景：过度的酒精摄入会导致诸多的肝脏疾病, 然而目前尚无有效的防治药物。前期研究发现鹿茸干细胞能够显著改善肝纤维化, 推测其 治疗作用可能是通过旁分泌效应产生的。目的：研究鹿茸干细胞的主要旁分泌物质——外泌体对小鼠急性肝损伤的预防作用及其机制。方法：40只C57BL6小鼠随机分为对照组、模型组、骨髓间充质干细胞外泌体预防组、鹿茸干细胞外泌体预防组, 每组10只。2个外泌体 预防组连续7 d给予相应外泌体进行干预, 模型组给予PBS干预, 然后给予体积分数为50%的酒精(15 mL/kg)灌胃1次建立急性酒精性肝损伤 模型。灌胃后24 h, 计算肝指数、检测肝损伤及氧化还原指标、评价肝组织病理病变、检测炎症因子和NF-κB信号通路相关基因的表达水 平。结果与结论：①鹿茸干细胞来源外泌体显著减轻了肝损伤的程度, 包括改善体质量、降低血清中谷丙转氨酶和谷草转氨酶水平、改善肝组 织病理病变、促进肝实质细胞增殖分裂以及提高抗氧化水平(谷胱甘肽过氧化物酶和超氧化物歧化酶水平升高, 丙二醛水平降低), 且效果 强于骨髓间充质干细胞来源外泌体；②进一步研究发现, 鹿茸干细胞来源外泌体显著降低了肝组织中白细胞介素1β、白细胞介素6和肿瘤 坏死因子α的mRNA表达水平, 以及NF-κB信号通路相关基因(p65、p-p65、IKB和p-IKB)的蛋白表达水平；③这说明鹿茸干细胞来源外泌体能 够起到保护肝脏的作用, 减轻酒精所造成的肝损伤, 其作用的发挥可能是通过靶向抑制NF-κB信号通路实现的。 [ABSTRACT FROM AUTHOR]

Oxidative stress, inflammatory response, and gut-liver axis dysbiosis have been suggested as the primarily involved in the pathogenesis of alcoholic liver injury. Previous research established that yeast extract (YE) has antioxidant, immuneboosting or microbiota-regulating properties. However, there is currently lack of information regarding the efficacy of YE on alcoholic liver injury. This study seeks to obtain data that will help to address this research gap using a Wistar male rat experimental model. Histologic and biochemical analysis results showed that the groups treated with both low-dose yeast extract (YEL) and high-dose yeast extract (YEH) had lower degrees of alcohol-induced liver injury. The abundance of Peptococcus and Ruminococcus reduced in the low-dose yeast extract (YEL) group, while that of Peptococcus, Romboutsia, Parasutterella, and Faecalibaculum reduced in the high-dose (YEH) group. Furthermore, Spearman analysis showed that the gut microbes were significantly associated with several liver-related indicators. For the analysis of differential metabolites and enriched pathways in the YEL group, the abundance of lysophosphatidylcholine (16:0/0:0) significantly increased, and then the levels of histamine, adenosine and 5' -adenine nucleotide were remarkedly elevated in the YEH group. These findings suggest that both high and low doses of YE can have different protective effects on liver injury in alcoholic liver disease (ALD) rats, in addition to improving gut microbiota disorder. Besides, high-dose YE has been found to be more effective than low-dose YE in metabolic regulation, as well as in dealing with oxidative stress and inflammatory responses. [ABSTRACT FROM AUTHOR]

[Objectives] This study was conducted to explore the optimization of ultrasonic-assisted organic solvent extraction of pomegranate peel polyphenols (PPPs), and to study the protective effect of PPPs on acute alcoholic liver injury in mice. [Methods] The optimal extraction conditions of PPPs were determined by single factor and orthogonal experiments, and an acute alcoholic liver injury model in mice was established. Bifendate was used as the positive control group to investigate the protective effect of low, medium and high doses of PPPs on acute alcoholic liver injury. [Results] The optimum extraction process parameters were followed as 60% ethanol concentration, solid-liquid ratio of 1 : 40 (w/v), extraction temperature of 50°C, and extraction time of 1.5 h, and the yield was 1.42%. The results of animal experiments showed that PPPs could effectively reduce the degree of alcoholic liver injury in mice, reduce the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and reduce the inflammation and necrosis of liver tissue in mice. Meanwhile, the total polyphenols from pomegranate peel also significantly reduced the expression levels of malondialdehyde (MDA), tumor necrosis factor (TNF-α) and interleukin-6 (IL-6) in mice, and increased the levels of superoxide dismutase (SOD) and reduced glutathione (GSH) in liver tissue of mice, indicating its antioxidant and anti-inflammatory effects, further illustrating its protective effect on alcoholic liver injury. [Conclusions] PPPs could reduce the expression levels of TNF-α, IL-6 and MDA in mice, and increase the expression levels of SOD and GSH to achieve the protective effect on acute alcoholic liver injury in mice. This study will provide new ideas for the development of new anti-alcoholic liver injury drug resources. [ABSTRACT FROM AUTHOR]