Experimentally assessing rifaximin's impact on liver inflammation in MASH, suggesting alternative mechanisms of action.
Key Points
The study aims to investigate the effects of rifaximin on inflammation and fibrosis in a model of metabolic dysfunction-associated steato-hepatitis (MASH).
Three groups of mice were assigned to receive different diets: normal, Western, and Western with rifaximin.
Liver function and serum levels of inflammatory markers (TNF-α, IL-1β, IL-6, LPS) were measured after 12 weeks.
Liver specimens were examined for pathological changes, lipid deposition, and fibrosis.
Faecal samples were analyzed for ethanol content and specific bacteria populations were isolated and tested for rifaximin sensitivity.
Rifaximin significantly reduced serum levels of TNF-α, IL-1β, IL-6, and LPS in mice on a Western diet.
There was a marked decrease in liver histology changes, fibrosis, and lipid content due to rifaximin treatment.
Expressions of p53, GFAP, CD68, and TLR-4 in the liver were reduced with rifaximin administration.
Faecal ethanol levels and numbers of ethanol-producing bacteria were unchanged despite rifaximin treatment.
Bacteria isolated from the rifaximin-treated group exhibited rifaximin resistance.