(1) Replication method 6-8 weeks old ApoE gene-deficient mice (strain C57BL/6J), half male and half, weighing 18-20g, fed with ω (fat) = 21%, ω (cholesterol) = 0.15% "Western type diet" feed (60CO sterilized irradiation treatment), the feeding condition is level 2, the room temperature is maintained at 22-24 ℃, and the relative humidity is 50%. The animal’s orbital blood was collected, and anticoagulant separated serum was used for blood lipid testing. The mice were sacrificed at 20 weeks, the heart and aorta were taken out under aseptic conditions, and fixed with 10% formaldehyde. After 20 weeks of feeding, obvious atherosclerotic plaques have formed in the aortic roots of the mice, the intima is obviously thickened, the subendothelial macrophages have gathered, and more foam cells and fibrous cap formation can be seen; after continuing feeding for 13 weeks The lesions were further aggravated. Obvious atherosclerotic plaque formation can be seen in the root of the aorta by HE staining. Foam cells and lipid cores are obvious, fibrous caps are thin, macrophages can be gathered locally, the vascular media structure is severely damaged, and lipid erosion , Atrophy and calcification, showing the characteristics of vulnerable plaque. This model can also be fed with a high-fat diet containing 2% cholesterol for 16 weeks. After 16 weeks, the serum lipid level will increase, and typical atherosclerotic plaques containing a lot of foam cells are formed in the aortic sinus valve and coronary arteries. Piece.
(2) Model features After the ApoE gene-deficient mice are fed a high-fat diet, obvious atherosclerotic plaques are formed in the aortic roots and coronary arteries. The model animal ApoE gene-deficient mice have a clear genetic background and strong reproduction , Lipid metabolism and plaque are similar to humans, and the animal is small, the dosage is small, and it is easy to feed and operate. It is an experimental atherosclerotic overall animal model suitable for screening anti-As drugs.
(3) Comparative medicine ApoE gene-deficient mice can spontaneously develop hyperlipidemia and atherosclerosis. After the model is formed, the blood total cholesterol level is 3~5g/L, which is close to the cholesterol level of human hyperlipidemia. Commonly used high-fat and high-cholesterol feeding animals have total cholesterol levels as high as 7-10g/L. The development of atherosclerosis in model mice includes lipid streaks to mature plaques covered with fibrous caps. As plaques are similar, and it is an ideal animal model for studying As plaques.