Supplementation of okra seed oil ameliorates ethanol-induced liver injury and modulates gut microbiota dysbiosis in mice

2019 ◽  
Vol 10 (10) ◽  
pp. 6385-6398 ◽  
Author(s):  
Jin Zhang ◽  
Yalong Lu ◽  
Xingbin Yang ◽  
Yan Zhao
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Liver Damage ◽  
Seed Oil ◽  
Gut Microbiota Dysbiosis

This study assesses the possible effects of dietary okra seed oil (OSO) consumption on attenuation of alcohol-induced liver damage and gut microbiota dysbiosis, and associated mechanisms in mice.

Gut dysbiosis correction contributes to the hepatoprotective effects of Thymus quinquecostatus Celak extract against alcohol through the gut–liver axis

2021 ◽  
Author(s):  
Xin Yan ◽  
Yu Wang ◽  
Xue-Yang Ren ◽  
Xiao-Yun Liu ◽  
Jia-Mu Ma ◽  
...  
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Alcoholic Liver Injury ◽  
Gut Dysbiosis ◽  
Hepatoprotective Effects ◽  
Gut Microbiota Dysbiosis

Gut microbiota dysbiosis correction contributes to the hepatoprotective effects of Thymus quinquecostatus Celak extract (TQE) against alcoholic liver injury through gut–liver axis modulation.

scholarly journals Gut Microbiota Was Involved in the Process of Liver Injury During Intra-Abdominal Hypertension

2021 ◽  
Vol 12 ◽  
Author(s):  
Zeyu Zhao ◽  
Zhengchang Guo ◽  
Zhengliang Yin ◽  
Yue Qiu ◽  
Bo Zhou
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Fecal Microbiota ◽  
Intestinal Damage ◽  
Abdominal Hypertension ◽  
Portal Veins ◽  
The Relationship ◽  
Abdominal Compartment ◽  
Gut Microbiota Dysbiosis

Background: Intestinal damage caused by intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) can lead to the ectopic gut microbiota, which can contribute to liver injury via portal veins. Therefore, it is speculated that gut microbiota disorder caused by IAH/ACS may result in liver injury. The relationship between gut microbiota and IAH/ACS-related liver injury was investigated in this study.Methods: A model of IAH was established in rats, and 16S rRNA sequencing was analyzed for gut microbiota in the feces of rats. The elimination of gut microbiota was completed by antibiotics gavage, and fecal microbiota transplantation (FMT) was used to change the composition of gut microbiota in rats.Results: In addition to the traditional cause of liver blood vessel compression, liver injury caused by IAH was also associated with gut microbiota dysbiosis. Gut microbiota clearance can relieve liver injury caused by IAH, while FMT from IAH-intervened rats can aggravate IAH-related liver injury.Conclusion: The gut microbiota was one of the most important factors contributing to the IAH-related liver injury, and the JNK/p38 signaling pathway was activated in this process.

scholarly journals Scutellarein Aggravated Carbon Tetrachloride-Induced Chronic Liver Injury in Gut Microbiota-Dysbiosis Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Zhimin Miao ◽  
Yong Lai ◽  
Yingying Zhao ◽  
Lingmin Chen ◽  
Jianeng Zhou ◽  
...  
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Relative Abundance ◽  
Function Analysis ◽  
Chronic Liver ◽  
Hepatoprotective Effect ◽  
Chronic Liver Injury ◽  
Cyp2e1 Expression ◽  
Factor Α ◽  
Gut Microbiota Dysbiosis

Scutellarein (SCU) is an herbal flavonoid, showing hepatoprotective potentials. The study was aimed to investigate whether the hepatoprotective effect of SCU is dependent on the integrity of gut microbiota. Mice received repeated intraperitoneal injections of CCl4, followed with or without SCU treatment (15, 30, and 60 mg/kg). Gut microbial community of mice was disrupted by administrating a cocktail of antibiotics (ampicillin, neomycin sulfate, metronidazole, and vancomycin) in drinking water. The results showed SCU plus antibiotics aggravated CCl4-induced chronic liver injury, as demonstrated by liver function analysis, histological analysis, and TUNEL assay. SCU activated CYP2E1 expression and worsened CYP2E1-mediated lipid peroxidation and oxidative stress as coadministered with antibiotics. Moreover, when gut microbiota was disrupted by antibiotics, SCU activated IκBα/NF-κB pathway and promoted the release of subsequent proinflammatory cytokines including interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α). Remarkably, the 16 S rRNA sequencing demonstrated that SCU greatly decreased the relative abundance of Bifidobacterium and Lactobacillus and increased the relative abundance of Enterococcus in gut microbiota-dysbiosis mice. Spearman correlation analysis showed that Lactobacillus was positively correlated with SOD and negatively correlated with AST. Collectively, the hepatoprotective effect of SCU is reversed under antibiotics intervention, which may partly involve the activation of CYP2E1 and IκBα/NF-κB pathway and diminishment of Lactobacillus.

Perfluorooctanoic acid-induced liver injury is potentially associated with gut microbiota dysbiosis

Chemosphere ◽  
2021 ◽  
Vol 266 ◽  
pp. 129004
Author(s):  
Gang Wang ◽  
Ruili Pan ◽  
Xi Liang ◽  
Xiaobing Wu ◽  
Yanmin Wu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Perfluorooctanoic Acid ◽  
Gut Microbiota Dysbiosis

scholarly journals Gut Microbiota Participates in Antithyroid Drug Induced Liver Injury Through the Lipopolysaccharide Related Signaling Pathway

2020 ◽  
Vol 11 ◽  
Author(s):  
Jiayu Sun ◽  
Fuya Zhao ◽  
Baiqiang Lin ◽  
Jing Feng ◽  
Xin Wu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Antithyroid Drug ◽  
Intestinal Barrier ◽  
Antithyroid Drugs ◽  
Sprague Dawley ◽  
Cross Sectional ◽  
Comparison Results ◽  
Gut Microbiota Dysbiosis ◽  
Microbiota Structure

Background: Drugs can alter the gut microbiota structure, and gut microbiota dysbiosis in turn is correlated with drug side effects through the intestinal endotoxemia hypothesis. Whether antithyroid drugs (including methimazole and propylthiouracil) cause gut microbiota dysbiosis and whether the gut microbiota is correlated with antithyroid drugs induced liver injury is unknown.Methods: Initial Graves’ disease patients were randomly divided into the methimazole group (n = 20) and the propylthiouracil group (n = 20) and were followed up every 2 weeks; 50 healthy controls were also included. The structure and function of gut microbiota were compared from the cross sectional and longitudinal levels. The correlation between the gut microbiota and clinical parameters was also determined. In addition, Sprague-Dawley rats were randomly allotted into six groups, including four drug groups, which received daily doses of methimazole (1.5 mg/kg/day; 2.5 mg/kg/day) or propylthiouracil (7.5 mg/kg/day; 12.5 mg/kg/day) by oral gavage, and two control groups received the vehicle. In addition to the indexes mentioned above, intestinal barrier-related indexes were also performed.Results: Cross sectional and longitudinal comparison results from both clinical trials and animal studies indicate that antithyroid drugs altered gut microbiota structure; and the liver function related indexes all increased which correlated with gut microbiota. In addition, lipopolysaccharide-related pathways and the lipopolysaccharide concentration in feces and serum all increased after antithyroid drugs administration. These results consistent with the destroyed intestinal barrier in animal study after antithyroid drugs administration.Conclusion: We verified that antithyroid drugs altered gut microbiota structure and that the gut microbiota may in turn be correlated with antithyroid drugs-induced liver injury through the intestinal endotoxemia hypothesis.

scholarly journals Dietary switch to Western diet induces hypothalamic adaptation associated with gut microbiota dysbiosis in rats

2021 ◽  
Author(s):  
Mélanie Fouesnard ◽  
Johanna Zoppi ◽  
Mélanie Petera ◽  
Léa Le Gleau ◽  
Carole Migné ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Western Diet ◽  
Dietary Switch ◽  
Gut Microbiota Dysbiosis

scholarly journals Constipation induced gut microbiota dysbiosis exacerbates experimental autoimmune encephalomyelitis in C57BL/6 mice

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiuli Lin ◽  
Yingying Liu ◽  
Lili Ma ◽  
Xiaomeng Ma ◽  
Liping Shen ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Gut Microbiota ◽  
Blood Brain Barrier ◽  
Intestinal Barrier ◽  
Brain Barrier ◽  
Autoimmune Encephalomyelitis ◽  
Gm Csf ◽  
Blood Brain ◽  
Gut Microbiota Dysbiosis ◽  
Experimental Autoimmune

Abstract Background Constipation is a common gastrointestinal dysfunction which has a potential impact on people's immune state and their quality of life. Here we investigated the effects of constipation on experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Methods Constipation was induced by loperamide in female C57BL/6 mice. The alternations of gut microbiota, permeability of intestinal barrier and blood–brain barrier, and histopathology of colon were assessed after constipation induction. EAE was induced in the constipation mice. Fecal microbiota transplantation (FMT) was performed from constipation mice into microbiota-depleted mice. Clinical scores, histopathology of inflammation and demyelination, Treg/Th17 and Treg17/Teff17 imbalance both in the peripheral lymphatic organs and central nervous system, cytokines include TGF-β, GM-CSF, IL-10, IL-17A, IL-17F, IL-21, IL-22, and IL-23 in serum were assessed in different groups. Results Compared with the vehicle group, the constipation mice showed gut microbiota dysbiosis, colon inflammation and injury, and increased permeability of intestinal barrier and blood–brain barrier. We found that the clinical and pathological scores of the constipation EAE mice were severer than that of the EAE mice. Compared with the EAE mice, the constipation EAE mice showed reduced percentage of Treg and Treg17 cells, increased percentage of Th17 and Teff17 cells, and decreased ratio of Treg/Th17 and Treg17/Teff17 in the spleen, inguinal lymph nodes, brain, and spinal cord. Moreover, the serum levels of TGF-β, IL-10, and IL-21 were decreased while the GM-CSF, IL-17A, IL-17F, IL-22, and IL-23 were increased in the constipation EAE mice. In addition, these pathological processes could be transferred via their gut microbiota. Conclusions Our results verified that constipation induced gut microbiota dysbiosis exacerbated EAE via aggravating Treg/Th17 and Treg17/Teff17 imbalance and cytokines disturbance in C57BL/6 mice.

Sign in / Sign up

Export Citation Format

Share Document