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Updated: Mar 25, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
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.
Background And Purpose:
Numerous in vitro studies have suggested that digoxin suppresses inflammation and alters lipid metabolism. However, the effect of dioxin on atherosclerosis is poorly understood. The present study was conducted to determine whether digoxin affects the development of atherosclerosis in a murine model of atherosclerotic disease.
Experimental Approach:
Apolipoprotein E-deficient mice maintained on a Western-type diet were administered PBS (control), low-dose digoxin (1 mg · kg(-1) · day(-1)) or high-dose digoxin (2 mg · kg(-1) · day(-1)) via i.p. injection for 12 weeks.
Key Results:
Digoxin dose-dependently reduced atherosclerotic lesion formation and plasma lipid levels (reductions of 41% in total cholesterol, 54% in triglycerides and 20% in low-density lipoprotein cholesterol in the high-dose digoxin-treated group). Moreover, treatment with digoxin markedly attenuated IL-17A expression and IL-17A-related inflammatory responses and increased the abundance of regulatory T cells (Tregs).
Conclusions And Implications:
Our data demonstrate that digoxin acts as a specific antagonist of retinoid-related orphan receptor-γ to decrease atherosclerosis by suppressing lipid levels and IL-17A-related inflammatory responses.
Insights
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.
