Related Experiment Video
Updated: Jul 19, 2026
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
A novel inhibitory effect of naloxone on macrophage activation and atherosclerosis formation in mice
Shu-Lin Liu1, Yi-Heng Li, Guey-Yueh Shi
1Department of Biochemistry and Molecular Biology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Objectives:
We investigated whether naloxone could reduce macrophage activation and influence atherosclerotic lesion formation in mice.
Background:
Macrophages play an important role in the inflammatory process in atherosclerosis. Naloxone could inhibit activation of microglia, the resident macrophage in the nervous system.
Methods:
The anti-inflammatory effect of naloxone was evaluated by stimulating the macrophage cell culture and FVB mice with lipopolysaccharide or oxidized low-density lipoprotein with and without naloxone pretreatment. Apolipoprotein-E (apoE)-deficient mice received naloxone injection for 10 weeks, and the severity of aortic atherosclerosis was measured. The left common carotid arteries of C57BL/6 mice were ligated near the carotid bifurcation. The mice then received naloxone injection for 4 weeks after ligation, and the severity of neointima formation was evaluated.
Results:
Naloxone pretreatment significantly suppressed the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-6, monocyte chemoattractant protein-1, and superoxide in macrophages after stimulation. In FVB mice, naloxone reduced the TNF-alpha level in circulation, inflammatory cell infiltration in lungs, and superoxide production in aorta. Naloxone injection significantly decreased the severity of aortic atherosclerosis in the apoE-deficient mice and carotid neointima formation in the C57BL/6 mice after ligation.
Conclusions:
Naloxone, with its novel anti-inflammatory effect, significantly reduces atherosclerosis and neointima formation in mice.
Insights
Naloxone significantly reduced inflammation and atherosclerosis in mice. This study shows naloxone
Area of Science:
- Immunology and cardiovascular research.
- Pharmacology of anti-inflammatory agents.
Background:
- Macrophages are key mediators of inflammation in atherosclerosis.
- Naloxone has demonstrated inhibitory effects on microglial activation.
Purpose of the Study:
- To determine if naloxone can decrease macrophage activation.
- To assess naloxone's impact on atherosclerotic lesion development in mice.
Main Methods:
- Macrophage cell cultures and FVB mice were stimulated with LPS or oxLDL, with/without naloxone.
- Apolipoprotein-E deficient mice and C57BL/6 mice underwent surgical procedures and naloxone treatment.
- Atherosclerosis and neointima formation were quantified.
Main Results:
- Naloxone suppressed inflammatory cytokine and superoxide production in macrophages.
- In vivo, naloxone reduced circulating TNF-alpha, lung inflammation, and aortic superoxide.
- Naloxone treatment significantly attenuated aortic atherosclerosis and carotid neointima formation.
Conclusions:
- Naloxone exhibits a novel anti-inflammatory effect.
- Naloxone effectively reduces atherosclerosis and neointima formation in murine models.
Related Concept Videos
01:38Inflammation
01:26Atherosclerosis III: Management