Camel milk modulates ethanol-induced changes in the gut microbiome and transcriptome in a mouse model of acute alcoholic liver disease

Liang, Ming; Qiao, X.R.; Li, Yang; Siren, Dalai; He, Jing; Hải, Lê Thanh; Guo, Fucheng; Xiao, Yuchen

doi:10.3168/jds.2019-17247

Cited by 27 publications

(26 citation statements)

References 45 publications

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“…Clinical trials have showed that the abundance of the intestinal microflora of ALD patients will change [44]. In this experiment, our results showed that in the intestinal flora of alcohol-treated mice, the abundance of harmful bacteria (norank_f_Muribaculaceae and un-classified_p_Firmicutes) increased and the abundance of beneficial bacteria (Akkermansia) decreased, which were consistent with the results of previous studies [45,46]. After treatment with a high dose of AP, the proportion of gut microbiota in ALD mice significantly improved, and the abundance of harmful bacteria decreased.…”

Section: Discussionsupporting

confidence: 92%

Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice

Zhou

Zhang

Zhao

et al. 2021

Foods

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Astragalus, a medical and edible plant in China, shows several bioactive properties. However, the role of astragalus in attenuating alcoholic liver disease (ALD) is less clear. The objective of this project is to investigate the improving effect of astragalus saponins (AS) and astragalus polysaccharides (AP), which are the two primary constituents in astragalus on hepatic injury induced by alcohol, and the potential mechanisms of action. Different doses of AS (50 and 100 mg/kg bw) and AP (300 and 600 mg/kg bw) were orally given to alcohol-treated mice for four weeks. The results demonstrated that both AP and AS could reverse the increase of the levels of TC, TG, FFA, and LDL-C in serum, and the decrease of serum HDL-C content, as well as the elevation of hepatic TC and TG levels induced by alcohol. The activities of AST, ALT, ALP, and γ-GT in ALD mice were raised after AP and AS supplementation. The antioxidant markers (SOD, CAT, GSH, and GSH-Px) were obviously augmented and the pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) and hepatic histological variations were alleviated by AP and AS, which was in line with the levels of oxidative stress-associated genes (Keap1, Nfe2l2, Nqo1, and Hmox1) and inflammation-associated genes (Tlr4, Myd88 and Nfkb1). In addition, AS exerted a more efficient effect than AP and the results presented dose proportionality. Moreover, AS and AP could modulate the intestinal microbiota disturbance induced by alcohol. Overall, AS and AP administration could ameliorate lipid accumulation in the serum and liver, as well as hepatic function, oxidative stress, inflammatory response, and gut flora disorders in mice as a result of alcohol.

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Section: Discussionsupporting

confidence: 92%

Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice

Zhou

Zhang

Zhao

et al. 2021

Foods

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“…Li et al (2020) used berberine to regulate gut microbes to induce the expansion of immune cells to combat ALD. Ming et al (2020) found that camel milk could alleviate the gut dysbiosis caused by acute alcohol, thereby alleviating liver inflammation. Ferrere et al (2017) found that gut microbes raised the sensitivity of alcohol-fed mice to ALD, and fecal microbiota transplantation or intake of prebiotics could prevent alcohol-induced liver damage in mice with ALD via regulating the gut microbiota structure.…”

Section: Introductionmentioning

confidence: 99%

Intake of Bifidobacterium lactis Probio-M8 fermented milk protects against alcoholic liver disease

Yang

Kang³

et al. 2022

Journal of Dairy Science

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Alcoholic liver disease (ALD) is a liver disease caused by long-term heavy drinking, which is characterized by increased inflammation and oxidative stress in the liver and gut dysbiosis. The purpose of this study was to investigate the protective effect of administering ordinary and probiotic-(containing the Bifidobacterium animalis ssp. lactis Probio-M8 strain; M8) fermented milk to rats. Several biochemical parameters and the fecal metagenomes were monitored before (d 0) and after (d 42) the intervention. Our results confirmed that alcohol could cause significant changes in the liver levels of the proinflammatory cytokine IL-1β, antioxidation indicators, and liver function-related indicators; meanwhile, the gut bacterial and viral microbiota were disrupted with significant reduction in microbial diversity and richness. Feeding the rats with Probio-M8-fermented milk effectively maintained the gut microbiota stability, reduced liver inflammation and oxidative stress, and mitigated liver damages in ALD. Moreover, the Probio-M8-fermented milk reversed alcohol-induced dysbiosis by restoring the gut microbiota diversity, richness, and composition. Four predicted fecal metabolites (inositol, tryptophan, cortisol, and vitamin K2) increased after the intervention, which might help regulate liver metabolism and alleviate ALD-related symptoms. In short, our data supported that consuming Probio-M8-fermented milk effectively mitigated ALD. The protective effect against ALD could be related to changes in the gut microbiome after probiotic-fermented milk consumption. However, such observation and the causal relationship among probiotic milk consumption, changes in gut microbiome, and disease alleviation would still need to be further confirmed. Nevertheless, this study has shown in a rat model that consuming probiotic-fermented milk could protect against ALD.

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“…This research confirmed that CXCL1 mRNA was the target of miR-532-5p in CI/RI-induced SH-SY5Y cells. CXCL1 is over-expressed in several human diseases and is a member of the chemotactic superfamily [ 21 , 22 ]. CXCL1 promotes inflammation and progression of several cancers [ 23 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-532-5p protects against cerebral ischemia-reperfusion injury by directly targeting CXCL1

Shi

Zhao

et al. 2021

Aging

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We investigated the function of microRNA (miR)-532-5p in cerebral ischemia-reperfusion injury (CI/RI) and the underlying mechanisms using oxygen-glucose deprivation and reperfusion (OGD/R)-treated SH-SY5Y cells and middle cerebral artery occlusion (MCAO) model rats. MiR-532-5p levels were significantly downregulated in OGD/R-treated SH-SY5Y cells and the brain tissues of MCAO model rats. MiR-532-5p overexpression significantly reduced apoptosis, reactive oxygen species (ROS), and inflammation in the OGD/R-induced SH-SY5Y cells. Bioinformatics analysis using the targetscan and miRDB databases as well as dual luciferase reporter assays confirmed that miR-532-5p directly binds to the 3’UTR of C-X-C Motif Ligand 1 (CXCL1). Methylation-specific PCR (MSP) analysis showed that miR-532-5p expression was reduced in OGD/R-treated SH-SY5Y cells because of miR-532-5p promoter hypermethylation. Moreover, 5-azacytidine, a methylation inhibitor, restored miR-532-5p expression in OGD/R-treated SH-SY5Y cells. Brain tissues of MCAO model rats showed significantly increased cerebral infarction areas, cerebral water, neuronal apoptosis, and activated CXCL1/CXCR2/NF-κB signaling, but these effects were alleviated by intraventricular injection of miR-532-5p agomir. These findings demonstrate that miR-532-5p overexpression significantly reduces in vitro and in vivo CI/RI by targeting CXCL1. Thus, miR-532-5p is a potential therapeutic target for patients with CI/RI.

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Camel milk modulates ethanol-induced changes in the gut microbiome and transcriptome in a mouse model of acute alcoholic liver disease

Cited by 27 publications

References 45 publications

Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice

Astragalus Polysaccharides and Saponins Alleviate Liver Injury and Regulate Gut Microbiota in Alcohol Liver Disease Mice

Intake of Bifidobacterium lactis Probio-M8 fermented milk protects against alcoholic liver disease

MicroRNA-532-5p protects against cerebral ischemia-reperfusion injury by directly targeting CXCL1

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