OBJECTIVE： To study the preventive effect of resveratrol on model mice and improvement effect on model golden hamsters （shorter for hamsters） with hyperlipidemia. METHODS： Hyperlipidemia animal models were induced by using high-fat and high-cholesterol diet. Mice and hamsters were both randomly divided into model group and resveratrol low-dose， medium-dose， high-dose groups （40， 80， 160 mg/kg for mice， 25， 50， 100 mg/kg for hamsters）， 10 in each group. 10 corresponding animals were selected as normal control group. Except that normal control group was fed normal diet and intragastrically administrated normal saline， other mice were intragastrically administrated relevant medicines when fed high-fat and high-cholesterol diet； other hamsters were firstly modeled for 2 weeks and intragastrically administrated relevant medicines after modeling. High-fat and high-cholesterol diet was fed during administration. It was administrated for 4 weeks. Total cholesterol （TC） and low density lipoprotein cholesterol （LDL-C） levels in serum of mice and hamsters were detected every week. After 4 weeks， pre-protein converting enzyme subtilisin 9 （PCSK9） mRNA and protein expression， microRNA-27a （miRNA-27a） expression in serum of mice and hamsters， and low density lipoprotein receptor （LDLR） protein expression in liver tissue of mice were detected. RESULTS： Compared with normal control group， the TC， LDL-C， PCSK9 mRNA and protein， miRNA-27a levels of mice in model group were obviously increased after 2 weeks of administration （P＜0.05）； LDLR protein level in liver tissue was obviously decreased （P＜0.05）. TC， LDL-C， PCSK9 mRNA and protein， miRNA-27a levels of hamsters in model group were obviously increased （P＜0.05）. Compared with model group， above-mentioned indexes of mice and hamsters in each administration group were obviously improved （P＜0.05）， which were positively correlated with dose. CONCLUSIONS： Resveratrol has preventive effect on model mice and improvement effect on model golden hamsters with hyperlipidemia. The mechanism may be down-regulating miRNA-27a expression and PCSK9 protein expression in serum， to increase LDLR protein level in liver tissue， and finally reduce LDL-C level.