title: [Protective effect of Saccharomyces boulardii against intestinal mucosal barrier injury in rats with nonalcoholic fatty liver disease].
abstract: Objective:To investigate the protective effect of Saccharomyces boulardii against intestinal mucosal barrier injury in rats with nonalcoholic fatty liver disease (NAFLD).Methods:A total of 36 healthy male Sprague-Dawley rats with a mean body weight of 180±20 g were randomly divided into control group, model group, and treatment group, with 12 rats in each group, after adaptive feeding for 1 week. The rats in the control group were given basic feed, and those in the model group and treatment group were given high-fat feed. After 12 weeks of feeding, the treatment group was given Saccharomyces boulardii (75×108CFU/kg/d) by gavage, and those in the control group and model group were given isotonic saline by gavage. At the 20th week, blood samples were taken from the abdominal aorta to measure the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG), intestinal fatty acid binding protein (IFABP), tumor necrosis factor-α (TNF-α), and endotoxins. The liver pathological changes, intestinal histopathological changes, and expression of occludin in the intestinal mucosa were observed. Fecal samples were collected to measure the changes in Escherichia coli and Bacteroides. A one-way analysis of variance and the SNK test were used for comparison between multiple groups, and the rank sum test was used as the non-parametric test.Results:Compared with the control group, the model group had significantly higher body weight, liver mass, and liver index (P< 0.05), and compared with the model group, the treatment group had significant reductions in body weight, liver mass, and liver index (P< 0.05). The model group had significant increases in TG, ALT, and AST compared with the control group (P< 0.05), the treatment group had a significant reduction in AST compared with the model group (P< 0.05), and the treatment group had slight reductions in TG and ALT compared with the model group (P> 0.05). Compared with the control group, the model group had significant increases in the levels of endotoxin, TNF-α, and IFABP (P< 0.05), and the treatment group had significant reductions in the levels of endotoxin, TNF-α, and IFABP (P< 0.05). Liver tissue staining showed that the model group had significantly increased hepatocyte steatosis compared with the control group (P< 0.05), and that the treatment group had significantly reduced hepatocyte steatosis compared with the model group (P< 0.05). The intestinal villi in the control group had ordered arrangement and a complete structure; in the model group, the intestinal villi were shortened with local shedding and a lack of ordered arrangement; compared with the model group, the treatment group had mild edema and ordered arrangements of the intestinal villi. The model group had a significantly reduced level of occludin protein compared with the control group (P< 0.05), and the treatment group had a slight increase compared with the model group. The model group had a significantly increased number of Escherichia coli and a significantly reduced number of Bacteroides compared with the control group (P< 0.05), and the treatment group had a significantly reduced number of Escherichia coli and a significantly increased number of Bacteroides compared with the model group (P< 0.05).Conclusion:High-fat diet can successfully induce NAFLD in rats, and intervention with Saccharomyces boulardii can reduce body weight and improve hepatocyte steatosis. Saccharomyces boulardii can reduce endotoxemia in NAFLD rats and thus alleviate inflammatory response. Saccharomyces boulardii can also adjust the proportion of Escherichia coli and Bacteroides in the intestine of NAFLD rats.
authors.affiliation: Hebei General Hospital Department of Gastroenterology, Shijiazhuang 050051, China.
authors.forename: Y T
authors.initials: YT
authors.lastname: Liu
authors.affiliation: Hebei General Hospital, Shijiazhuang 050051, China.
authors.forename: Y Q
authors.initials: YQ
authors.lastname: Li
authors.affiliation: Hebei General Hospital Department of Gastroenterology, Shijiazhuang 050051, China.
authors.forename: Y Z
authors.initials: YZ
authors.lastname: Wang
mesh_terms: D000410:Alanine Transaminase; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D059305:Diet, High-Fat; D004731:Endotoxins; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology; D007421:Intestine, Small / Q000378:metabolism / Q000382:microbiology; D008297:Male; D065626:Non-alcoholic Fatty Liver Disease / Q000382:microbiology* / Q000628:therapy*; D062793:Occludin / Q000378:metabolism; D019936:Probiotics / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D000069983:Saccharomyces boulardii; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D004731:Endotoxins; D062793:Occludin; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase