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Objective: To investigate the protective effects of mannan oligosaccharide (MOS) and partially hydrolyzed guar gum (PHGG) on liver injury induced by long-term alcohol intake in mice. Methods: Mice were randomly divided into control (Ctrl), model (EtOH), positive control (PC, silymarin at 86 mg/(kg·d)), MOS intervention (2 000 mg/(kg·d)) and PHGG intervention (2 000 mg/(kg·d)) groups. A Lieber-DeCarli model of chronic alcoholic liver injury (ALD) was established in this study. After five weeks of feeding, the levels of liver function, oxidative stress and inflammatory factors were measured. Hematoxylin-eosin (HE) staining and oil red O (ORO) staining were used to observe hepatic histopathological alterations. The mRNA and protein expression levels of ileal tight junction proteins (zonula occludens-1 and occludin) were detected by real-time fluorescence quantitative polymerase chain reaction (qPCR) and immunofluorescence staining, respectively. The hepatic lipopolysaccharide (LPS) level was quantitatively determined by enzyme-linked immunosorbent assay (ELISA). Besides, the contents of acetic acid, propionic acid, isobutyric acid, butyric acid, isovaleric acid, valeric acid and caproic acid in fecal samples were quantitatively analyzed by gas chromatography-mass spectrometry (GC-MS). Results: Supplementation of MOS and PHGG could significantly attenuate hepatic steatosis, lipid accumulation, oxidative stress and inflammation induced by long-term ethanol exposure. Additionally, compared with the EtOH group, MOS and PHGG intake markedly improved liver function and intestinal barrier function, inhibited intestinal LPS leakage, and increased intestinal short-chain fatty acids (SCFAs) levels. Conclusion: Guar gum-derived MOS and PHGG could effectively alleviate chronic ALD in mice by enhancing intestinal integrity and regulating intestinal SCFA levels.

Huangjiu is rich in low-molecular-weight peptides and has an umami taste. In order for its umami peptides to be discovered, huangjiu was subjected to ultrafiltration, ethanol precipitation, and macroporous resin purification processes. The target fractions were gathered according to sensory evaluation. Subsequently, we used peptidomics to identify the sum of 4158 peptides in most umami fractions. Finally, six novel umami peptides (DTYNPR, TYNPR, SYNPR, RFRQGD, NFHHGD, and FHHGD) and five umami-enhancing peptides (TYNPR, SYNPR, NFHHGD, FHHGD, and TVDGPSH) were filtered via virtual screening, molecular docking, and sensory verification. Moreover, the structure–activity relationship was discussed using computational approaches. Docking analysis showed that all umami peptides tend to bind with T1R1 through hydrogen bonds and hydrophobic forces, which involve key residues HIS71, ASP147, ARG151, TYR220, SER276, and ALA302. The active site calculation revealed that the positions of the key umami residues D and R in the terminal may cause taste differences in identified peptides. [ABSTRACT FROM AUTHOR]

Different alcoholic beverages and drinking patterns might exert divergent impacts on alcoholic liver disease (ALD) progression. Whether the abundant non-alcoholic components (NAC) in fermented wine could alleviate ethanol (EtOH)-induced adverse influences on the liver remains unknown. Hence, the chronic ALD mouse model was established to compare the effects of Huangjiu (a typical fermented wine) and EtOH feeding on the liver, intestinal barrier, gut microbiota, and intestinal short-chain fatty acids (SCFAs) content. Although Huangjiu intake led to slight hepatic steatosis, it mitigated oxidative stress, inflammation, and intestinal damage relative to EtOH intake. In comparison with EtOH feeding, Huangjiu significantly improved the intestinal barrier integrity and reduced hepatic lipopolysaccharide levels by up-regulating the expression of intestinal tight junction proteins (ZO-1 and occludin) and antimicrobial activity peptides (Reg3β and Reg3γ). The administration of Huangjiu NAC partially restored alcohol-induced gut microbiota dysbiosis via recovering the abundance of Lactobacillus, Faecalibaculum, and Akkermansia. Moreover, mice receiving Huangjiu showed higher SCFAs levels (such as acetic acid and butyric acid) than those receiving EtOH. Huangjiu consumption resulted in lower hepatotoxicity than pure EtOH, at the same alcohol dose. The NAC in Huangjiu might attenuate the progression of ALD by regulating intestinal barrier function and microbiota-meditated gut ecology. [ABSTRACT FROM AUTHOR]

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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.)

Osteoarthritis has become one of the main diseases affecting the life of many elderly people with high incidence of disability, and local chronic inflammation in the joint cavity is the most crucial pathological feature of osteoarthritis. Astilbin is the main active component in a variety of natural plants such as Hypericum perforatum and Sarcandra glabra, which possess antioxidant and anti‐inflammatory effects. At present, there is no study about the protective effect of Astilbin for osteoarthritis. The purpose of this study was to investigate the effect of Astilbin in human OA chondrocytes and mouse OA model, which was established by surgery‐mediated destabilization of the medial meniscus (DMM). In vitro, we found that Astilbin pre‐treatment inhibited lipopolysaccharide (LPS)‐induced overproduction of inflammation‐correlated cytokines such as nitric oxide (NO), prostaglandin E2 (PGE2), tumour necrosis factor α (TNF‐α) and interleukin 6 (IL‐6), and suppressed overexpression of inflammatory enzymes such as inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX‐2). Astilbin, on the other hand, prevented the LPS‐induced degradation of extracellular matrix (ECM) by down‐regulating MMP13 (matrix metalloproteinases 13) and ADAMTS5 (a disintegrin and metalloproteinase with thrombospondin motifs 5). Moreover, by inhibiting the formation of the TLR4/MD‐2/LPS complex, Astilbin blocked LPS‐induced activation of TLR4/NF‐κB signalling cascade. In vivo, Astilbin showed the chondro‐protective effect in the surgical‐induced OA mouse models. In conclusion, our findings provided evidence that develops Astilbin as a potential therapeutic drug for OA patients. [ABSTRACT FROM AUTHOR]