Objective To establish animal model of hemorrhagic endogenous collateral wind syndrome that is up to clinical practice

with mobility and general applicability. Methods Apo E（-/-） gene knock out mice were fed with high-fat diet and received arteria carotis casing technique at the 12 th week. Mice were randomly divided into control group

stress group

Compound group

stress + Compound group after operation. Four weeks after operation

conducted intraperitoneal injection of lipopolysaccharide 1mg/kg on all mice

twice per week

for 8 weeks. Eight weeks after operation

stress group

stress + Compound group were given limited mental stimulation

4 h per day

for4 weeks in total; ten weeks after operation

mice in the Compound group

the stress + Compound group received intraperitoneal injection of Compound 48/80 0. 5 mg/kg

once every other day

4 times in total. Blood lipid and pathomorphology of plaque were examined and plaque areas

rate of stenosis of vascular lumen were calculated 12 weeks after operation. Compared lipid

collagen

smooth muscle cells and monocytes/macrophages level in plague and calculated vulnerability index of plaque. Results There was no statistical significance in difference of blood lipid of mice in each group（ P > 0. 05）. Compared with the control group

bleeding in plaque in the Compound group remarkably increased and there was statistical significance in difference of whole pathomorphism condition of plaque in the stress +Compound group（ P < 0. 05）. The difference between plague areas

stenosis rate of vessel lumen

lipid and smooth muscle cells level in plaque in each group had no statistical significance（ P > 0. 05）. Monocytes/macrophages level in the stress + Compound group and the Compound group remarkably increased compared with the control group（ P <0. 05）. Collagen level in the plaque in the stress + Compound group decreased compared with other groups

while vulnerability index increased（ P < 0. 05）. Conclusion Adopting lipopolysaccharide + stress + Compound 48/80 together to establish mouse model of hemorrhagic endogenous collateral wind syndrome had relatively high vulnerability index of plaque and bleeding rate in plaque. It could be used as the best modeling method of animal model of hemorrhagic endogenous collateral wind syndrome.