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Updated: Sep 27, 2026
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
No effect of cyclooxygenase inhibition on plaque size in atherosclerosis-prone mice
Mette Olesen1, Elizabeth Kwong, Arguello Meztli
1Department of Cardiology, Institute of Experimental Clinical Research, Aarhus University Hospital (Skejby), DK-8200 Aarhus N, Denmark.
Objective:
To study the role of cyclooxygenase (COX) inhibition on the development of advanced atherosclerosis in apolipoprotein E-deficient (apoE(-/-)) mice.
Design:
Sixty apoE(-/-) mice were divided into three groups: a control group, a group fed standard mouse chow supplemented with 0.0067% (wt/wt) MF Tricyclic (selective COX-2 inhibitor), and a group fed the diet supplemented with 0.0134% (wt/wt) sulindac (non-selective COX inhibitor). Four months later, the mice were killed and the atherosclerotic plaque area in the aortic root was measured.
Results:
Mean body weights did not differ at any time. The MF Tricyclic and sulindac groups had drug plasma levels of 1.31 +/- 0.11 and 0.84 +/- 0.23 micro g/ml, respectively. Plasma total cholesterol and triglyceride values were similar in all three groups. A small difference in plasma levels of high-density lipoprotein cholesterol was found between the groups (p = 0.03). Advanced atherosclerotic plaques were present in mice from all three groups, but there was no difference in mean plaque size between the groups (p = 0.9).
Conclusion:
Neither selective COX-2 nor non-selective COX inhibition influenced the development of advanced atherosclerosis in apoE(-/-) mice.
Insights
Cyclooxygenase (COX) inhibition did not impact atherosclerosis development in apolipoprotein E-deficient mice. Neither selective COX-2 nor non-selective COX inhibitors altered advanced plaque size in this advanced atherosclerosis model.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Immunology
Background:
- Atherosclerosis is a chronic inflammatory disease.
- Cyclooxygenase (COX) enzymes play a role in inflammation.
- Inhibition of COX may modulate atherosclerotic plaque development.
Purpose of the Study:
- To investigate the effect of cyclooxygenase (COX) inhibition on advanced atherosclerosis.
- To determine if selective COX-2 inhibition or non-selective COX inhibition impacts plaque development in apolipoprotein E-deficient (apoE(-/-)) mice.
Main Methods:
- Sixty apoE(-/-) mice were divided into control, selective COX-2 inhibitor (MF Tricyclic), and non-selective COX inhibitor (sulindac) groups.
- Mice were fed supplemented diets for four months.
- Atherosclerotic plaque area in the aortic root was measured post-mortem.
Main Results:
- No significant differences in mean body weight, plasma total cholesterol, or triglyceride levels were observed between groups.
- A minor difference in high-density lipoprotein cholesterol was noted (p = 0.03).
- Advanced atherosclerotic plaques were present in all groups, with no significant difference in mean plaque size (p = 0.9).
Conclusions:
- Neither selective COX-2 inhibition nor non-selective COX inhibition influenced the development of advanced atherosclerosis in apoE(-/-) mice.
- These findings suggest that COX inhibition may not be a therapeutic target for advanced atherosclerosis in this model.
