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Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
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Digoxin reduces atherosclerosis in apolipoprotein E-deficient mice.
Huairui Shi1, Xiaobo Mao1, Yucheng Zhong1
1The Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
British Journal of Pharmacology
|February 17, 2016
Summary
Digoxin significantly reduced atherosclerosis in mice by lowering cholesterol and triglyceride levels. It also decreased inflammation by inhibiting IL-17A and boosting regulatory T cells (Tregs).
Area of Science:
- Cardiovascular Research
- Immunology
- Pharmacology
Background:
- In vitro studies suggest digoxin impacts inflammation and lipid metabolism.
- The role of digoxin in atherosclerosis development remains unclear.
Purpose of the Study:
- To investigate the effect of digoxin on atherosclerosis progression.
- To evaluate digoxin's impact in a murine model of atherosclerotic disease.
Main Methods:
- Apolipoprotein E-deficient mice were fed a Western-type diet.
- Mice received intraperitoneal injections of PBS (control), low-dose, or high-dose digoxin for 12 weeks.
Main Results:
- Digoxin dose-dependently reduced atherosclerotic lesion formation.
- Significant reductions in total cholesterol, triglycerides, and LDL cholesterol were observed.
- Digoxin attenuated IL-17A expression, inflammatory responses, and increased regulatory T cell (Treg) abundance.
Conclusions:
- Digoxin acts as a retinoid-related orphan receptor-γ antagonist.
- Digoxin decreases atherosclerosis by suppressing lipid levels and IL-17A-related inflammation.
