To investigate the regulatory effect of emodin on lipid profile in dietinduced hyperlipidemic rats and elucidate the molecular mechanisms involved, male SD rats were randomly divided into 4 groups (8 rats for each group) including control group, hyperlipidemia group, simvastatin group and emodin group.The control group was given normal diet, and others were given diet rich in cholesterol. In the meantime, the simvastatin group and emodin group was orally administrated with simvastatin（10 mg/kg） and emodin （10 mg/kg），respectively. After continous gavage for 38 days, the lipid profile was investigated by the content of serum total cholesterol(TC), triglyceride(TG), low density lipoprotein cholesterol (LDLC) and high density lipoprotein cholesterol (HDLC).The atherogenic index (AI) of each group was calculated and compared. Pathological features of liver histology were observed. Thoracic aortas were isolated and divided into two sections, one for in vitro incubation and detection of total nitric oxide (NO) content in supernatant, the other for measuring the mRNA expression level of endothelial nitric oxide synthase(eNOS) by realtime fluorescence quantification PCR and the protein expression level by western blotting. The results showed that emodin markedly attenuated the increased serum TC, TG and LDLC induced by hypercholesterolemic diet. Compared with the hyperlipidemia group, emodin significantly reduced AI value. Liver histopathology examination showed that emodin observably reduced the degree of steatosis in hepatocytes of hyperlipidemic rats. Emodin significantly increased the secretion of NO in vitro, and also upregulated both the mRNA and protein expression levels of eNOS in thoracic aortas. The results of the present experiment indicate that emodin can lower serum TC,TG,LDLC and reduce the atherogenic properties of dietary choleaterol in rats. Its antihyperlipidemic function may be due to upregulating the level of eNOS/NO system and protecting the blood vessel endothelium.