In connection to intestinal and hepatic disorders, the gut-liver axis has lately been extensively studied. Bile acid (BA) receptors, such as farnesoid-X-receptor (FXR), pregnane-X-receptor (PXR), and G-protein-coupled-receptor (GPCR), are key players in a variety of metabolic processes, as well as inflammation and fibrosis. The purpose of this study is to look at the effects of intestinal inflammation on liver health, specifically FXR, PXR, and TGR5 expression. It is also thought about how to enhance liver health by lowering intestinal inflammation. The modulation of BA receptors in inflammatory bowel disease (IBD) juvenile patients’ inflamed colonic tissues is investigated. An animal model of dextran sodium sulphate (DSS) colitis was created. Co-cultures with the Caco2 and HepG2 cell lines were established. Real-time PCR and immunohistochemistry were used to look for changes in BA receptors in IBD pediatric patients’ biopsies. Histology revealed inflammatory cell infiltration in the livers of DSS animals, with FXR and PXR levels considerably lower and oxidative stress elevated. When Caco2 was exposed to inflammatory stimuli, BA receptor expression in HepG2 was reduced. These effects on liver cells were decreased when Caco2 was treated with dipotassium glycyrrhizate (DPG). Patients with inflamed colons have changed FXR, PXR, and TGR5 expression.
This data clearly shows that gut inflammation impacts hepatic cells by changing BA receptor expression and boosting pro-inflammatory cytokine and oxidative stress production. As a result, decreasing gut inflammation is essential not just for improving intestinal illness but also for protecting the liver.