Sorry, you need to enable JavaScript to visit this website.

Colonic inflammation accelerates the progression of liver disease: A protective role of dipotassium glycyrrhizate

TitleColonic inflammation accelerates the progression of liver disease: A protective role of dipotassium glycyrrhizate
Publication TypeArticolo su Rivista peer-reviewed
Year of Publication2021
AuthorsFiaschini, Noemi, Negroni Anna, Palone Francesca, Vitali Roberta, Colantoni Eleonora, Laudadio Ilaria, Mancuso Mariateresa, Cucchiara Salvatore, and Stronati Laura
JournalDigestive and Liver Disease
Date PublishedJan-12-2021
Keywordsalanine aminotransferase, alanine aminotransferase blood level, alpha smooth muscle actin, animal, animal experiment, animal model, animal tissue, Animals, article, bacterial translocation, C57BL mouse, complication, controlled study, cryopyrin, dextran sulfate sodium-induced colitis, diet, dipotassium glycyrrhizate, disease activity, disease exacerbation, disease model, Disease Models, drinking water, drug efficacy, fluorescence in situ hybridization, fructose, Glucose, High-Fat, Immunofluorescence, immunofluorescence assay, immunohistochemistry, Inbred C57BL, inflammation, interleukin 6, lipid diet, Liver, liver fibrosis, liver histology, liver protective agent, male, messenger RNA, Mice, mouse, Non-alcoholic Fatty Liver Disease, nonalcoholic fatty liver, nonalcoholic steatohepatitis, nonhuman, Pathology, protein expression, real time polymerase chain reaction, steatosis, toll like receptor 4, transforming growth factor beta, Tumor Necrosis Factor, unclassified drug

Background: The incidence of non-alcoholic fatty liver disease (NAFLD) and its more severe and progressive form, non-alcoholic steatohepatitis (NASH) is increasing worldwide. Gut inflammation seems to concur to the pathogenesis of NASH. No drugs are currently approved for NASH treatment. Aims: To investigate if inflamed gut directly contributes to the progression of NASH through gut epithelial and vascular barrier impairment and to evaluate the efficacy of dipotassium glycyrrhizate (DPG) to improve the liver disease. Methods: A NASH model was set up by feeding mice, for 8 and 13 weeks, with high fat diet with high fructose and glucose (HFD-FG) supplemented periodically with dextran sulfate sodium (DSS) in drinking water. A group was also treated with DPG by gavage. Histological, immunohistochemical and molecular analysis were performed. Results: DSS-induced colitis increased steatosis, inflammatory (IL-6, TNFα, NLRP3, MCP-1) as well as fibrotic (TGF-β, α-SMA) mediator expression in HFD-FG mice. Beneficial effect of DPG was associated with restoration of intestinal epithelial and vascular barriers, evaluated respectively by ZO-1 and PV-1 expression, that are known to limit bacterial translocation. Conclusion: Colonic inflammation strongly contributes to the progression of NASH, likely by favouring bacterial translocation. DPG treatment could represent a novel strategy to reduce liver injury. © 2021


cited By 0

Short TitleDigestive and Liver Disease
Citation Key9463