Comparison Log 2025-10-12 09:19:52.863257 mwtab Python Library Version: 1.2.5 Source: https://www.metabolomicsworkbench.org/rest/study/analysis_id/AN006974/mwtab/... Study ID: ST004196 Analysis ID: AN006974 Status: Inconsistent Sections "PROJECT" contain missmatched items: {('PROJECT_SUMMARY', 'Fluoride is an environmental pollutant that causes intestinal barrier damage, but the role of the "gut microbiota-RhoA/ROCK-cytoskeleton" axis in this process remains unclear. The aim of this project is to investigate the damage mechanism of high fluoride exposure on the intestinal barrier in mice. Focusing on the core objective of how high fluoride affects the intestinal barrier through the gut microbiota-mediated "RhoA/ROCK - cytoskeleton remodeling" axis, the study combines metagenomic approaches and leverages untargeted metabolomic analysis to reveal the gut microbiota dysbiosis and significant changes in intestinal metabolites induced by high fluoride. It clarifies the variation of cytoskeleton-related differential metabolites and screens out the key bacterial species that are strongly associated with the phenotypic characteristics of intestinal barrier damage, cytoskeletal core proteins, key tight junction proteins, and RhoA/ROCK pathway molecules in mice. In doing so, this research provides a new perspective for studying the mechanism of fluoride-induced intestinal barrier damage and lays a foundation for the prevention of fluoride-related intestinal diseases.'), ('PROJECT_SUMMARY', 'Fluoride is an environmental pollutant that causes intestinal barrier damage, but the role of the gut microbiota-RhoA/ROCK-cytoskeleton axis in this process remains unclear. The aim of this project is to investigate the damage mechanism of high fluoride exposure on the intestinal barrier in mice. Focusing on the core objective of how high fluoride affects the intestinal barrier through the gut microbiota-mediated RhoA/ROCK - cytoskeleton remodeling axis, the study combines metagenomic approaches and leverages untargeted metabolomic analysis to reveal the gut microbiota dysbiosis and significant changes in intestinal metabolites induced by high fluoride. It clarifies the variation of cytoskeleton-related differential metabolites and screens out the key bacterial species that are strongly associated with the phenotypic characteristics of intestinal barrier damage, cytoskeletal core proteins, key tight junction proteins, and RhoA/ROCK pathway molecules in mice. In doing so, this research provides a new perspective for studying the mechanism of fluoride-induced intestinal barrier damage and lays a foundation for the prevention of fluoride-related intestinal diseases.')} Sections "STUDY" contain missmatched items: {('STUDY_SUMMARY', 'Our study establishes an acute high-fluoride exposure model by gavaging 3-week-old C57BL/6J mice with 0 (control, C), 12 (low fluoride, FL), or 24 mg/kg (high fluoride, FH) sodium fluoride (NaF) for 8 weeks (n=10 per group), with standardized housing conditions (22±2℃, 12 h light/dark cycle). After euthanasia, ileal tissues, ileal contents, and serum were collected for histological, molecular, metagenomic, and non-targeted metabolomic analyses. Histological and biochemical results showed that high fluoride (FH group) increased ileal crypt depth, elevated serum intestinal permeability indicators (LPS, DAO, D-LA), and reduced ileal antioxidant capacity (decreased T-AOC, GSH, SOD; increased H₂O₂). Immunofluorescence, Western blotting, and transmission electron microscopy revealed that high fluoride activated the RhoA/ROCK pathway (upregulated RhoA, ROCK1/2, p-MLC), induced abnormal rearrangement and aggregation of F-actin (P<0.001 vs C), and disrupted the apical junctional complex (AJC)—manifested by downregulated expression and cytoplasmic translocation of ZO-1, Claudin-1, and β-catenin. Metagenomic analysis of ileal contents indicated high fluoride-induced gut microbiota dysbiosis, with reduced abundance of Akkermansia muciniphila and enrichment of Lactobacillus johnsonii; two key species (Bifidobacterium sp. SO1 and Schaalia turicensis) were screened, showing strong correlations with intestinal barrier phenotypes, RhoA/ROCK pathway molecules, and cytoskeleton-related metabolites. Non-targeted metabolomics identified 620 differential metabolites, with 11 linked to cytoskeleton function; high fluoride enriched linoleic acid metabolism (upregulated 9-HODE, 13-KODE; P<0.05 vs C) and sphingolipid metabolism (downregulated sphingosine) pathways. These findings confirm that high fluoride impairs the mouse intestinal barrier via the gut microbiota-mediated "RhoA/ROCK-cytoskeleton remodeling" axis, providing novel insights into fluoride-induced intestinal toxicity mechanisms and a basis for preventing fluoride-related intestinal diseases.'), ('STUDY_SUMMARY', 'Our study establishes an acute high-fluoride exposure model by gavaging 3-week-old C57BL/6J mice with 0 (control, C), 12 (low fluoride, FL), or 24 mg/kg (high fluoride, FH) sodium fluoride (NaF) for 8 weeks (n=10 per group), with standardized housing conditions (22±2℃, 12 h light/dark cycle). After euthanasia, ileal tissues, ileal contents, and serum were collected for histological, molecular, metagenomic, and non-targeted metabolomic analyses. Histological and biochemical results showed that high fluoride (FH group) increased ileal crypt depth, elevated serum intestinal permeability indicators (LPS, DAO, D-LA), and reduced ileal antioxidant capacity (decreased T-AOC, GSH, SOD; increased H₂O₂). Immunofluorescence, Western blotting, and transmission electron microscopy revealed that high fluoride activated the RhoA/ROCK pathway (upregulated RhoA, ROCK1/2, p-MLC), induced abnormal rearrangement and aggregation of F-actin (P<0.001 vs C), and disrupted the apical junctional complex (AJC)—manifested by downregulated expression and cytoplasmic translocation of ZO-1, Claudin-1, and β-catenin. Metagenomic analysis of ileal contents indicated high fluoride-induced gut microbiota dysbiosis, with reduced abundance of Akkermansia muciniphila and enrichment of Lactobacillus johnsonii; two key species (Bifidobacterium sp. SO1 and Schaalia turicensis) were screened, showing strong correlations with intestinal barrier phenotypes, RhoA/ROCK pathway molecules, and cytoskeleton-related metabolites. Non-targeted metabolomics identified 620 differential metabolites, with 11 linked to cytoskeleton function; high fluoride enriched linoleic acid metabolism (upregulated 9-HODE, 13-KODE; P<0.05 vs C) and sphingolipid metabolism (downregulated sphingosine) pathways. These findings confirm that high fluoride impairs the mouse intestinal barrier via the gut microbiota-mediated RhoA/ROCK-cytoskeleton remodeling axis, providing novel insights into fluoride-induced intestinal toxicity mechanisms and a basis for preventing fluoride-related intestinal diseases.')} Unable to find '_DATA' block in given files.