The probiotic effects of AB23A on high-fat-diet-induced non-alcoholic fatty liver disease in mice may be associated with suppressing the serum levels of lipopolysaccharides and branched-chain amino acids

Xia, Fan; Xiang, Shijian; Chen, Zhijuan; Song, Limei; Li, Yuxin; Liao, Ziqiong; Ge, Bingchen; Zhou, Benjie

doi:10.1016/j.abb.2021.109080

Cited by 39 publications

(29 citation statements)

References 41 publications

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“…AB23A displays a protective effect on intestinal permeability by upregulating and restoring occludin and ZO-1 expression and distribution. These findings are consistent with our previous results in NAFLD mice showing that AB23A maintains intestinal barrier integrity by inhibiting HFD-induced downregulation of TJ expressions, including ZO-1 and occludin ( Xia et al, 2021 ).…”

Section: Discussionsupporting

confidence: 93%

“…Moreover, A novel study indicated that AB23A enhances intestinal permeability and microecological disorders in mice with colitis-associated cancer (CAC) ( Zhu et al, 2021 ). Our previous study also has confirmed that AB23A could inhibit high fat diet-induced down-regulation of TJ-related proteins in NAFLD mice ( Xia et al, 2021 ). Even so, AB23A mechanism on intestinal permeability is poorly known.…”

Section: Introductionsupporting

confidence: 57%

“…Fatty liver diseases comprising steatohepatitis (NASH) and non-alcoholic fatty liver disease (NAFLD) are related to elevated intestinal barrier permeability and translocation of bacteria or bacterial products into the blood circulation, according to accumulating studies ( Mouries et al, 2019 ). Past investigations have demonstrated that AB23A maintains the intestinal barrier integrity and reduces the endotoxin level in HFD-induced NAFLD or colitis-associated cancer (CAC) mice ( Xia et al, 2021 ; Zhu et al, 2021 ). Even so, AB23A protective mechanisms on the function of the intestinal barrier remain poorly understood.…”

Section: Discussionmentioning

confidence: 99%

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Alisol B 23-Acetate Ameliorates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction by Inhibiting TLR4-NOX1/ROS Signaling Pathway in Caco-2 Cells

Xia

Deng

et al. 2022

Front. Pharmacol.

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Alisol B 23-Acetate (AB23A) is a naturally occurring triterpenoid, which can be indicated in the rhizome of medicinal and dietary plants from Alisma species. Previous studies have demonstrated that AB23A could inhibit intestinal permeability by regulating tight junction (TJ)-related proteins. Even so, the AB23A protective mechanism against intestinal barrier dysfunction remains poorly understood. This investigation seeks to evaluate the AB23A protective effects on intestinal barrier dysfunction and determine the mechanisms for restoring intestinal barrier dysfunction in LPS-stimulated Caco-2 monolayers. According to our findings, AB23A attenuated the inflammation by reducing pro-inflammatory cytokines production like IL-6, TNF-α, IL-1β, and prevented the paracellular permeability by inhibiting the disruption of TJ in LPS-induced Caco-2 monolayers after treated with LPS. AB23A also inhibited LPS-induced TLR4, NOX1 overexpression and subsequent ROS generation in Caco-2 monolayers. Transfected with NOX1-specific shRNA diminished the up-regulating AB23A effect on ZO-1 and occludin expression. Moreover, transfected with shRNA of TLR4 not only enhanced ZO-1 and occludin expression but attenuated NOX1 expression and ROS generation. Therefore, AB23A ameliorates LPS-induced intestinal barrier dysfunction by inhibiting TLR4-NOX1/ROS signaling pathway in Caco-2 monolayers, suggesting that AB23A may have positive impact on maintaining the intestinal barrier’s integrity.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

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Alisol B 23-Acetate Ameliorates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction by Inhibiting TLR4-NOX1/ROS Signaling Pathway in Caco-2 Cells

Xia

Deng

et al. 2022

Front. Pharmacol.

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“…At the genus level, compared with the MOD group, COST reduced the relative abundance of the Desulfovibrio genera and increased the relative abundance of Bacteroides , Lachnospiraceae, and Akkermansia . Among them, Desulfovibrio was pathogenic bacteria and closely related to the occurrence of obesity and hyperlipidemia [ 29 , 30 ]. In a large number of studies, the Bacteroides strain has also been proven to regulate the redox level in the intestinal tract, creating many favorable conditions for the host [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

The Ameliorative Effect of COST on Diet-Induced Lipid Metabolism Disorders by Regulating Intestinal Microbiota

et al. 2022

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(1) Background: Chitosan oligosaccharides, with an average molecular weight ≤ 1000 Da (COST), is a natural marine product that has the potential to improve intestinal microflora and resist lipid metabolism disorders. (2) Methods: First, by establishing a mice model of lipid metabolism disorder induced by a high fat and high sugar diet, it is proven that COST can reduce lipid metabolism disorder, which may play a role in regulating intestinal microorganisms. Then, the key role of COST in the treatment of intestinal microorganisms is further confirmed through the method of COST-treated feces and fecal bacteria transplantation. (3) Conclusions: intestinal microbiota plays a key role in COST inhibition of lipid metabolism disorder induced by a high fat and high sugar diet. In particular, COST may play a central regulatory role in microbiota, including Bacteroides, Akkermansia, and Desulfovibrio. Taken together, our work suggests that COST may improve the composition of gut microbes, increase the abundance of beneficial bacteria, improve lipid metabolism disorders, and inhibit the development of metabolic disorders.

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“…There is not much literature on Ileibacterium, with only one characterized species, I. valens, in 2017. 39 So far, I. valens has been seen to increase in abundance after dietary changes, [39][40][41][42] and it has been associated with a few immunological and host physiological parameters. 42 Our results here suggest that it may be a very actively replicating member of the mouse gut microbiota, though its specific roles in the gut are yet to be determined.…”

Section: Discussionmentioning

confidence: 99%

Actively replicating gut bacteria identified by 5-ethynyl-2’-deoxyuridine (EdU) click chemistry and cell sorting

Beauchemin

Hunter

Maurice³

2022

Preprint

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The composition of the intestinal bacterial community is well described, but recent research suggests that the metabolism of these bacteria plays a larger role in health than which species are present. One fundamental aspect of gut bacterial metabolism that remains understudied is bacterial replication. Indeed, there exist few techniques which can identify actively replicating gut bacteria. In this study, we aimed to address this gap by adapting 5-ethynyl-2′-deoxyuridine (EdU) click chemistry (EdU-click), a metabolic labeling method, coupled with fluorescence-activated cell sorting and sequencing (FACS-Seq) to characterize replicating gut bacteria. We first used EdU-click with human gut bacterial isolates and show that many of them are amenable to this technique. We then optimized EdU-click and FACS-Seq for murine fecal bacteria and reveal that Prevotella UCG-001 and Ileibacterium are enriched in the replicating fraction. Finally, we labelled the actively replicating murine gut bacteria during exposure to cell wall-specific antibiotics in vitro. We show that regardless of the antibiotic used, the actively replicating bacteria largely consist of Ileibacterium, suggesting the resistance of this taxon to perturbations. Overall, we demonstrate how combining EdU-click and FACSeq can identify the actively replicating gut bacteria and their link with the composition of the whole community in both homeostatic and perturbed conditions. This technique will be instrumental in elucidating in situ bacterial replication dynamics in a variety of other ecological states, including colonization and species invasion, as well as for investigating the relationship between the replication and abundance of bacteria in complex communities.

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The probiotic effects of AB23A on high-fat-diet-induced non-alcoholic fatty liver disease in mice may be associated with suppressing the serum levels of lipopolysaccharides and branched-chain amino acids

Cited by 39 publications

References 41 publications

Alisol B 23-Acetate Ameliorates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction by Inhibiting TLR4-NOX1/ROS Signaling Pathway in Caco-2 Cells

Alisol B 23-Acetate Ameliorates Lipopolysaccharide-Induced Intestinal Barrier Dysfunction by Inhibiting TLR4-NOX1/ROS Signaling Pathway in Caco-2 Cells

The Ameliorative Effect of COST on Diet-Induced Lipid Metabolism Disorders by Regulating Intestinal Microbiota

Actively replicating gut bacteria identified by 5-ethynyl-2’-deoxyuridine (EdU) click chemistry and cell sorting

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