Dendrobium huoshanense Polysaccharide Improves High‐Fat Diet Induced Liver Injury by Regulating the Gut‐Liver Axis

Abstract

Dendrobium huoshanense is an important Traditional Chinese medicine that thickens the stomach and intestines. Its active ingredient Dendrobium huoshanense polysaccharide (DHP), was revealed to relieve the symptoms of liver injury. However, its mechanism of action remains poorly understood. This study aimed to investigate the mechanism of DHP in protecting the liver. The effects of DHP on lipid levels, liver function, and intestinal barrier function were investigated in mice with high‐fat diet‐induced liver damage. Changes in the gut flora and their metabolites were analyzed using 16S rRNA sequencing and metabolomics. The results showed that DHP reduced lipid levels, liver injury, and intestinal permeability. DHP altered the intestinal flora structure and increased the relative abundance of Bifidobacterium animalis and Clostridium disporicum. Furthermore, fecal metabolomics revealed that DHP altered fecal metabolites and significantly increased levels of gut‐derived metabolites, spermidine, and indole, which have been reported to inhibit liver injury and improve lipid metabolism and the intestinal barrier. Correlation analysis showed that spermidine and indole levels were significantly negatively correlated with liver injury‐related parameters and positively correlated with the intestinal species B. animalis enriched by DHP. Overall, this study confirmed that DHP prevented liver injury by regulating intestinal microbiota dysbiosis and fecal metabolites.

Puerarin Modulates Hepatic Farnesoid X Receptor and Gut Microbiota in High-Fat Diet-Induced Obese Mice

“…Clostridium celatum is a member of the Clostridia class, a diverse assembly encompassing both commensal and pathogenic strains. Beneficial clostridia contribute to gut homeostasis and the fermentation of dietary fiber; however, certain species may behave as opportunists, fostering inflammatory states and dysbiosis when proliferating under conditions such as a high-fat diet (HFD) [51]. The observed increase in the abundance of Clostridium celatum and other members of the Clostridia class in response to a high-fat diet (HFD) could potentially activate inflammatory pathways and compromise gut integrity.…”

“…The observed increase in the abundance of Clostridium celatum and other members of the Clostridia class in response to a high-fat diet (HFD) could potentially activate inflammatory pathways and compromise gut integrity. This disturbance in gut barrier function and immune system engagement may exacerbate systemic inflammation, predisposing individuals to metabolic disorders such as obesity [51]. TCA significantly decreased the relative abundance of three culturable species of commensal bacteria, Turicibacter sanguinis, Lactobacillus johnsonii, and Clostridium celatum, in both cecal contents and mucosal scrapings from the colon [52].…”