scholarly journals Mastiha ( Pistacia lentiscus ) Improves Gut Microbiota Diversity, Hepatic Steatosis, and Disease Activity in a Biopsy‐Confirmed Mouse Model of Advanced Non‐Alcoholic Steatohepatitis and Fibrosis

2019 ◽  
Vol 63 (24) ◽  
pp. 1900927 ◽  
Author(s):  
Aimo Kannt ◽  
Efstathia Papada ◽  
Claire Kammermeier ◽  
Giuseppe D'Auria ◽  
Nuria Jiménez‐Hernández ◽  
...  
2020 ◽  
Vol 35 (12) ◽  
pp. 2140-2150 ◽  
Author(s):  
Tomoki Kobayashi ◽  
Keishi Kanno ◽  
Phuong Thao Nguyen ◽  
Akiko Sugiyama ◽  
Akihiro Kawahara ◽  
...  

Author(s):  
Ming Zhang ◽  
Aoqiang Li ◽  
Qifang Yang ◽  
Jingyi Li ◽  
Lihua Wang ◽  
...  

It was recently shown that the gut microbiota of both depression patients and depression model animals is significantly altered, suggesting that gut microbes are closely related to depression. Here, we investigated the effects of Sophora alopecuroides L.-derived alkaloids on the gut microbiota of mice with depression-like behaviors. We first established a mouse model of depression via chronic unpredictable mild stress (CUMS) and detected changes in depression-like behaviors and depression-related indicators. Simultaneously, 16S rRNA sequencing was performed to investigate gut microbiota changes. Sophora alopecuroides L.-derived alkaloids improved depression-like behaviors and depression-related indicators in mice. The alkaloids decreased the gut microbiota diversity of CUMS mice and depleted intestinal differentially abundant “harmful” microbiota genera. Spearman analysis showed that there is a certain correlation between the differential microbiota (Lactobacillus, Helicobacter, Oscillospira, Odoribacter, Mucispirillum, Ruminococcus), depression-like behaviors, and depression-related indicators. Combined with the predictive analysis of gut microbiota function, these results indicate that alkaloids improve depression in mice through modulating gut microbiota.


2019 ◽  
Author(s):  
Thibaut Duparc ◽  
François Briand ◽  
Charlotte Trenteseaux ◽  
Jules Mérian ◽  
Guillaume Combes ◽  
...  

ABSTRACTAimNon-alcoholic steatohepatitis (NASH) is an emerging health problem worldwide. However, efficacious pharmacological treatment for NASH is lacking. A major issue for preclinical evaluation of potential therapeutics for NASH is the limited number of appropriate animal models, i.e., models that do not require long-term dietary intervention and adequately mimic disease progression in humans. The present study aimed to evaluate a 3-week dietary mouse model of NASH and to validate it by studying the effects of liraglutide, a compound in advanced clinical development for NASH.MethodsC57BL6/J mice were fed a diet high in fat (60%), cholesterol (1.25%) and cholic acid (0.5%) along with 2% hydroxypropyl-β-cyclodextrin in drinking water (HFCC-CDX diet). Histological and biological parameters were measured at 1 and 3 weeks. Following 1-week diet induction, liraglutide was administrated daily for 2 weeks, and then NASH-associated phenotypic aspects were evaluated in comparison with control mice.ResultsPrior to treatment with liraglutide, mice fed the HFCC-CDX diet for 1 week developed liver steatosis and had increased levels of oxidative-stress markers and hepatic and systemic inflammation. For mice not treated with liraglutide, these aspects were even more pronounced after 3 weeks of the dietary period, with additional liver insulin resistance and fibrosis. Liraglutide treatment corrected the diet-induced alterations in glucose metabolism and significantly reduced hepatic steatosis and inflammation.ConclusionThis study provides a novel 3-week dietary model of mice that rapidly develop NASH features, and this model will be suitable for evaluating the therapeutic efficacy of compounds in preclinical drug development for NASH.


2013 ◽  
Vol 47 (3) ◽  
pp. 137-149 ◽  
Author(s):  
Thomas Klein ◽  
Masato Fujii ◽  
Jan Sandel ◽  
Yuichiro Shibazaki ◽  
Kyoko Wakamatsu ◽  
...  

2019 ◽  
Vol 67 (7) ◽  
pp. 2098-2112 ◽  
Author(s):  
Alexandra Ntemiri ◽  
Céline Ribière ◽  
Catherine Stanton ◽  
R. Paul Ross ◽  
Eibhlís M. O’Connor ◽  
...  

2019 ◽  
Vol 10 (4) ◽  
pp. 413-424 ◽  
Author(s):  
C. Linninge ◽  
J. Xu ◽  
M.I. Bahl ◽  
S. Ahrné ◽  
G. Molin

Probiotics should bring ‘balance’ to the intestinal microbiota by stimulating beneficial bacteria, whilst mitigating adverse ones. Balance can also be interpreted as high alpha-diversity. Contrary, Escherichia coli is often regarded as an adverse component of the resident intestinal microbiota. The aim of the present study was to implement a mouse model for in vivo screening of Lactobacillus-strains for ability to increase gut-microbiota diversity and to mitigate E. coli. Mice were divided into six groups, two dietary control-groups and four groups administered strains of Lactobacillus fermentum and/or Lactobacillus plantarum. All animals were pre-treated with antibiotics, and E. coli in order to equalise the microbiota from the start. After 7 weeks of Lactobacillus administration, the animals were sacrificed: DNA was extracted from caecum tissue, and the microbiota composition was analysed with terminal restriction fragment length polymorphism (T-RFLP) and 16S rRNA gene sequencing. The diversity of the caecal microbiota decreased when the dietary carbohydrate source was limited to corn starch. Conversely, the diversity was restored by Lactobacillus-supplements. The tested combinations of two Lactobacillus strains exerted different influences, not only on the taxonomic level, but also on the inferred microbiome functions. The mixture of L. fermentum GOS47 and L. fermentum GOS1 showed potential for anti-inflammatory activity and short chain fatty acid production. On the other hand, co-administration of L. fermentum GOS57 and L. plantarum GOS42 significantly decreased the viable count of Enterobacteriaceae. These results warrant further investigation of the tested strains as candidates for probiotics. Furthermore, the findings demonstrated that the current experimental animal model is suitable for in vivo studies of the effect of bacterial supplements on the gut-microbiota.


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