Validation experiment designed to validate causal mechanisms targeting GPR109A in C57BL/6J mice. Primary outcome: Colonic GPR109A expression and intestinal barrier integrity
This experiment investigated the effects of ligature-induced periodontitis on intestinal inflammation and barrier function in mice. C57BL/6J mice were subjected to periodontal ligature placement under normal chow or high-fructose diet conditions. The study evaluated periodontal destruction using micro-CT and histological analysis, then assessed downstream effects on colonic GPR109A expression, intestinal epithelial integrity, and both local and systemic inflammatory responses. Multiple analytical techniques were employed including histology, immunostaining, qPCR, ELISA, and GC-MS/MS for short-chain fatty acid quantification. The experiment aimed to establish a mechanistic link between periodontitis and gut inflammation through microbiota-mediated pathways.
Ligature-induced periodontitis in mice, followed by micro-CT analysis, histological evaluation, qPCR, immunostaining, ELISA, and GC-MS/MS analysis of colonic contents
Periodontitis would downregulate GPR109A expression and disrupt intestinal barrier function
Significant changes in GPR109A expression, tight junction protein localization, and inflammatory markers
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