Objective To investigate whether glucagon-like peptide-1（GLP-1）（7-36） inhibits the progression of aortic atherosclerotic plaque in ApoE knockout(ApoE

-/-

) mice fed with high-fat diet and the effect of GLP-1（7-36） on the expressions of CD36 and acyl-coenzyme A:cholesterol acyltransferase 1（ACAT1） in macrophage-derived foam cells. Methods Forty male ApoE

-/-

mice（6-8 weeks old

weighing 18-20 g） were randomized equally into normal diet group

high-fat diet（model） group

GLP-1（7-36） group

and GLP-1（7-36）+Exendin（9-39） group. The area of the atherosclerotic plaque in the aortic root of the mice was determined using HE staining

oil red O staining

and immunohistochemical staining with CD36 and ACAT1 antibodies. In the cell experiment

the macrophages（RAW264.7 cells） were induced with oxidized low-density lipoprotein（ox-LDL） and treated with different concentrations of GLP-1（7-36）

alone or in combination with Exendin（9-39）. The expressions of CD36 and ACAT1 mRNAs and proteins in the cells was detected using RT-PCR and Western blotting

respectively. The levels of total cholesterol（TC）

free cholesterol（FC） and cholesterol ester（CE） in the cells were detected using high-performance liquid chromatography

and immunofluorescence analysis was performed to detect the expressions of CD36 and ACAT1 receptor proteins. Results Compared with the control mice

ApoE

-/-

mice on high-fat diet showed significantly higher expression levels of CD36 and ACAT1 at both the mRNA and protein levels in the aortic atherosclerotic plaques（P

<

0.05）. CD36 and ACAT1 expressions in the plaques were significantly lowered by treatment of the mice with GLP-1（7-36）（P

<

0.05）; the expression levels of CD36 and ACAT1 were significantly higher in GLP-1+Exendin group than in GLP-1 group（P

<

0.05）. HE and oil red O staining showed that in the model group

the mean proportion of the plaque area in the aortic intimal area was（30.3±3.8）%

which was significantly lowered to（15.1±4.3）% in GLP-1 group（P

<

0.05）; the ratio of the plaque area was（25.7±3.4）% in GLP-1+Exendin group

where significantly more numerous atherosclerotic plaques were observed below the intima as compared with GLP-1 group（P

<

0.05）. GLP-1（7-36） significantly decreased the percentage of CD36-and ACAT1-positive cells in the aorta of the mice（P

<

0.05）. Conclusion GLP-1 can reduce the accumulation of intracellular cholesterol by inhibiting the expression of CD36 and ACAT1 to suppress the foaming of macrophages

and thus inhibits the formation of atherosclerotic plaques.