Abstract
Objective To establish a stable and reliable mouse atherosclerotic (AS) model, and standardize principal process of AS model identification. Methods The mouse AS model was developed by feeding apolipoprotein E (ApoE) gene knockout mice (ApoE-/-) on high-fat diet (hfd). Sixteen weeks later, the body weight, blood sugar, blood pressure and blood lipid were determined, and aortas were stained with oil red O and hematoxylin to evaluate the AS plaque. Results Cholesterol [(20.09±1.02) mmol/L] and low density lipoprotein cholesterol [(6.84±0.65) mmol/L] of ApoE-/- mice with hfd were significantly increased as compared with that in C57BL/6J normal diet (nd) group [total cholesterol (TC): (2.04±0.07) mmol/L, LDL-C: (0.25±0.01) mmol/L, F=190.543, 82.795, P<0.01]. Oil Red O staining of entire aorta showed that AS lesion size in ApoE-/-+ hfd mice [(22.09±3.49)%] was dramatically increased as compared with that in ApoE-/-+ nd mice [(1.46±0.96)%, F=118.558, P<0.01]. Similar result was obtained from cross-sections of aortic root analysis. Hematoxylin and eosin (HE) staining of cross-sections of aorta root showed typical As plaques. Conclusion The hfd treatment successfully promoted AS development in ApoE-/- mice. The process of gene identification-general situation analysis-blood lipid analysis-morphologic analysis was established to verify AS model. The establishment of mouse AS model provides a valuable tool for the study of AS-related diseases in vivo. Key words: Atherosclerosis; Gene knock out mice; Low density lipoprotein; Cholesterol; Lorta
Published Version
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