Moreover, βCD-PRX treatment markedly suppressed hepatic mRNA expression of Ccl2 and profibrotic factors, along with their serum cytokine levels, in the NASH model (Fig. 4 F and Table S4) without remarkable impact on hepatic expression of genes related to cholesterol metabolism, de novo lipogenesis, β-oxidation, and glucose metabolism, except Mttp, which mediates very-low-density lipoprotein secretion from the livers (Fig. 4 F). This evidence concerns the gene PRX and metabolic dysfunction-associated steatohepatitis.