Our results showed that HNK significantly increased the mRNA expression of hepatic Pparα, Fabp5, Cpt1α, Acox, Scd-1, Gpat, and Mttp in mice with NASH, indicating that HNK could accelerate fatty acid β-oxidation by upregulating the mRNA expression of Pparα and its downstream target genes Acox, Fabp5, and Cpt1α; suppress fatty synthesis by increasing the mRNA expression of Scd-1, Gpat, and Mttp; and ultimately improve hepatic fat deposition. This evidence concerns the gene CPT1A and metabolic dysfunction-associated steatohepatitis.