Overall, isorhamnetin intervention through modulating the composition of BAs significantly upregulated FXR and BSEP protein expression in the liver, while notably downregulating SLCO1B3 expression (Figure 5E–G), thereby enhancing BA export from the liver to the intestine and reducing BAs reabsorption, improving bile acid metabolic balance and alleviating cholestasis, which enabled the liver to metabolize excess T-CHO, effectively slowing down the progression of NAFLD. This evidence concerns the gene NR1H4 and metabolic dysfunction-associated steatotic liver disease.