Proteceive Effect And Mechanism Of LGG In DSS-induced Inflammatory Bowel Disease In Mice

Inflammatory bowel disease?IBD?is a recurrent gastrointestinal disease with complex pathogenesis,characterized by intestinal mucosa damage and persistent intestinal inflammation.Lactobacillus rhamnosus GG?LGG?can be planted in the human intestine and has a regulatory effect on the intestinal flora.Some studies have pointed out that LGG has a certain protective effect in the onset of inflammatory bowel disease,but it is not clear whether long-term treat with LGG has a preventive protective effect on IBD and its mechanism of action.Objective:This study explores whether LGG has preventive protection effect on IBD and its mechanism of action through the acute IBD mouse model induced by dextran sodium sulfate?DSS?.Methods:C57BL/6 mice were randomly divided into control group,DSS group,LGG group,LGG+DSS group.During the 5-weeks trial period,the mice in the LGG group and LGG+DSS group were given 1×10⁹CFU/only LGG gastric,DSS group and LGG+DSS group mice given the same volume of MRS liquid culture medium every day,and in the last week of the experiment,the DSS group and LGG+DSS group were constructed with 3%DSS drinking water to construct an acute IBD model of the mice,analyzed the degree of colon tissue inflammation,the infiltration of inflammatory cells and the expression of the tight junction protein in the intestines,and combined with the effect of caco-2 cell in vitro testing of LGGs on intestinal permeability.Results:1.Compared with the DSS group of mice,LGG+DSS group mice significantly reduced the weight loss of the mice caused by DSS-induced IBD,and reduced the degree of inflammation of enteritis,inflammatory cell immersion and histological damage.2.DSS group mice in the colon tissue of the tight junction protein Occludin and Claudin-1 expression were significantly reduced,and LGG pre-treatment significantly increased the expression of the tight junction Occludin and Claudin-1 in the colon tissue of LGG+DSS group.3.In vitro culture treatment Of Caco-2,LPS or H₂O₂ treatment significantly inhibited the expression of Occludin and Claudin-1,and significantly reduced the resistance value of single-layer cells.LGGs pre-treatment and then giving LPS or H₂O₂treatment promotes a significant increasing of Occludin and Claudin-1 expression,while reducing the resistance value of single-layer cells.Conclusion:LGG pretreatment can prevent the protection of DSS-induced acute enteritis in mice,and LGG reduces intestinal permeability by regulating the expression of tight junction proteins in the intestine.We discusses the protective effect and mechanism of LGG in inflammatory bowel disease,and provides a theoretical basis for the application of LGG in inflammatory bowel disease.