The results showed that MLE significantly down-regulated the expression levels of lipid-related markers such as SREBP2, HMGCR, miR-33a, and CYP7A1 in the liver, inhibited lipid accumulation in a rat model of NAFLD, and attenuated liver injury, thereby exerting a protective effect during NAFLD treatment [42]. This evidence concerns the gene HMGCR and metabolic dysfunction-associated steatotic liver disease.