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Atherosclerosis animal model

Atherosclerosis animal model

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Atherosclerosis
Psychiatric & neurological disease models

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Experimental results

Experimental results

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Atherosclerosis

Introduction to the AS Mouse Model

Atherosclerosis animal models (AS) are typically established by combining a high‑fat diet with an inducing agent, thereby mimicking the vascular lesions caused by abnormal lipid metabolism in humans. In these models, blood lipid levels are markedly elevated, and lipid deposition and plaque formation occur on the luminal surfaces of vessels such as the aorta and coronary arteries, accompanied by intimal thickening and luminal narrowing; in some cases, plaque rupture and calcification can also be observed. These features allow for a faithful recapitulation of the onset and progression of atherosclerosis, making such models well suited for investigating underlying mechanisms and for drug development.

Aniphe BioLab’s AS Mouse Model Platform: Service Advantages

The platform boasts mature technology and standardized quality control, enabling efficient conduct of research related to atherosclerosis.

Comprehensive model coverage

Model stability

A mouse model was established by combining gene-edited mice with a high-fat diet, yielding typical phenotypes such as plaque formation and dyslipidemia, with excellent reproducibility.

Standardization of the modeling process

Full-process quality control

Standardized rearing and procedures, multi‑parameter verification, and reliable experimental data.

Multidimensional Evaluation System

Comprehensive testing

Equipped with a range of assessment tools, including lipid profiling, pathology, and imaging, it provides comprehensive monitoring throughout the entire disease course.

Adapted for multi-cycle studies

Flexible customization

The modeling protocol can be tailored on demand to accommodate a wide range of pharmacological efficacy and mechanistic studies.

Standardization of Data Delivery

One-stop service

The entire process is completed independently, ensuring high delivery efficiency and compliance with project requirements.

Modeling cycle

12 weeks

1  Laboratory animals

APOE mice

1  Positive drug

Lipid-modifying agents such as atorvastatin, rosuvastatin, and probucol are commonly used as positive control drugs and can effectively lower lipid levels and inhibit plaque progression.

1  Application areas

This model is primarily used to investigate the pathogenic mechanisms underlying lipid metabolism disorders, vascular inflammation, endothelial injury, and atherosclerotic plaque formation. It is widely applied in the screening of lipid‑lowering, anti‑atherosclerotic, and plaque‑stabilizing drugs, as well as in pharmacodynamic and safety evaluations. Additionally, it supports the validation of drug targets, the development of bioactive natural compounds, and the assessment of vascular‑protective intervention strategies.

Experimental results

Construction of an animal model of AS

APOE gene-knockout mice + high-fat diet induction; vascular endothelial injury method

Model characteristics: Mechanical injury directly induces intimal damage, enabling the rapid establishment of a well‑developed atherosclerotic model that markedly accelerates lipid and calcium deposition as well as the infiltration of inflammatory cells into the bloodstream, with a high surgical success rate. Alternatively, using gene‑knockout mice fed a high‑fat diet allows for controlled pathological progression, facilitating direct visualization of the entire disease‑development process.

Pathological staining results of model establishment

This set of histological sections represents the aortic pathology staining results in an atherosclerosis‑model mouse, allowing clear visualization of lesion characteristics under different staining methods:

In the figure, the aortic vessel walls all exhibit marked thickening, with an irregular lumen morphology. Lipid deposition and plaque formation are evident on the intimal surface; in some sections, plaques protrude into the lumen, leading to luminal stenosis. Different staining techniques—Oil Red O, Masson’s trichrome, and hematoxylin–eosin—highlight lipid content, collagen fibers, inflammatory cells, and other components, respectively, thereby clearly illustrating the typical pathological changes of the arterial wall characteristic of atherosclerosis and confirming the successful establishment of the model.

 

 

Atorvastatin (Ator) Treatment Data

01 Biochemical Test Results

Compared with the control group, after 10 weeks of intervention with low- and high-dose atorvastatin, the concentrations of LDL‑C, TC, and TG in mouse serum were all reduced, with a more pronounced reduction observed in the high‑dose group; these differences were statistically significant (P<0.05). No statistically significant differences were observed among the groups for GLU or HDL‑C concentrations.

 

 

02 Results of ORO Staining and HE Staining

0RO staining revealed prominent lipid deposition in the aortic endothelium of mice in the control group. In both the low‑dose and high‑dose Ator groups, lipid deposition was reduced, with a more pronounced effect observed in the high‑dose group; these differences were statistically significant (P<0.001). HE staining showed that the control group exhibited a larger plaque area on aortic cross‑section [(1.62±0.15) mm²], whereas the low‑dose and high‑dose Ator groups demonstrated significantly smaller plaque areas [(1.13±0.06) mm² and (0.83±0.07) mm², respectively]. The high‑dose group displayed superior efficacy, with statistically significant differences (P<0.001).

 

 

03 Western Blot Results

Ator downregulated the expression of inflammation‑related proteins (NLRP3, TNF‑α, IL‑6), oxidative stress‑related protein (iNOS), pro‑apoptotic proteins (caspase‑3, p53), and MMP‑7, while upregulating the expression of antioxidant proteins (SIRT3, SOD2), anti‑apoptotic protein (Bcl‑2), and Gα13. The effects were more pronounced in the high‑dose group, with statistically significant differences (P<0.05). The trends in mRNA expression of these proteins were consistent with the corresponding protein expression changes.

 

References: Atorvastatin enhances the stability of atherosclerotic plaques in ApoE‑/‑ mice by modulating MMP‑7/Gα13.