ABSTRACT: Objective This study aims to investigate the mechanism by which a traditional Chinese medicine compound, based on rice bran fatty alkanols, aids in reducing blood lipids by regulating hepatic cholesterol metabolism. Methods Thirty-six SD rats were randomly allocated into four groups: a normal control group, a hyperlipidemia model group, a positive control group treated with simvastatin, and three test substance groups receiving high, medium, or low doses of the traditional Chinese medicine compound. The normal control group was administered an equal volume of double-distilled water via gavage, while the remaining groups were given a fat emulsion to induce hyperlipidemia in SD rats. After four weeks of treatment with the designated substances, serum and liver lipid levels were assessed. Hematoxylin-eosin (HE) staining was performed to examine changes in liver tissue morphology, and oil red O staining was used to visualize lipid deposition. Real-time fluorescent quantitative polymerase chain reaction (qPCR) was utilized to quantify the mRNA expression levels of cholesterol 7α-hydroxylase (CYP7A1), low-density lipoprotein receptor (LDLR), and proprotein convertase subtilisin/kexin type 9 (PCSK9) in the liver. Results The test substance significantly decreased the levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) in the serum and liver of hyperlipidemic rats compared to the model group (P＜0.01, P＜0.001). HE and oil red O staining revealed that the test substance reduced fat accumulation in the liver and attenuated the degree of hepatocyte steatosis. Additionally, the test substance significantly upregulated the expression of CYP7A1 mRNA in the liver (P＜0.001) and downregulated the expression of PCSK9 mRNA (P＜0.01) compared to the model group. Conclusion The traditional Chinese medicine compound, consisting of rice bran fatty alkanols, hawthorn, and Panax notoginseng, effectively lowers blood lipids in hyperlipidemic rats, and its mechanism may involve the regulation of hepatic cholesterol uptake and utilization.