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Updated: Aug 12, 2025

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
Icariin alleviates atherosclerosis by regulating the miR-205-5p/ERBB4/AKT signaling pathway
Peng Huang1, Fengjun Wang2, Yibing Zhang3
1Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun, China.
Insights
Icariin (ICA) effectively treats atherosclerosis (AS) by reducing lipid accumulation and plaque formation. It also inhibits vascular smooth muscle cell proliferation and migration, potentially via miR-205-5p.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pharmacology
Background:
- Atherosclerosis (AS) poses a significant global health risk.
- Understanding therapeutic mechanisms for AS is crucial.
Purpose of the Study:
- To investigate the therapeutic effects of icariin (ICA) on atherosclerosis.
- To elucidate the underlying molecular mechanisms of ICA in AS treatment.
Main Methods:
- Atherosclerosis was modeled in ApoE-/- mice and human aortic vascular smooth muscle cells (HAVSMCs).
- Icariin treatment effects were assessed using lipid accumulation, plaque formation, cell viability, apoptosis, and migration assays.
- MicroRNA (miRNA) profiling and in silico analyses identified potential signaling pathways, including miR-205-5p.
Main Results:
- Icariin reduced blood lipid accumulation and plaque formation in AS mice.
- Icariin promoted apoptosis and inhibited migration in ox-LDL-induced HAVSMCs.
- The inhibitory effects of ICA on cell proliferation and migration were reversed by silencing miR-205-5p.
Conclusions:
- Icariin alleviates atherosclerosis by inhibiting proliferation and migration of vascular smooth muscle cells.
- The therapeutic action of icariin may be mediated by the upregulation of miR-205-5p.
Purpose:
Atherosclerosis (AS) is a cardiovascular disease that has become a major threat to public health worldwide. This study aims to elucidate the effect and mechanism of icariin (ICA) in treating atherosclerosis.
Methods:
ApoE-/- mouse AS modeling, ELISA, and hematoxylin-eosin staining were conducted to explore whether icariin has a therapeutic effect on AS. The microRNA (miRNA) chips for ICA treatment of ApoE-/- AS mice were developed; in silico analyses were performed, and signaling pathways were identified. Oxidized low-density lipoprotein (Ox-LDL) was used to induce human aortic vascular smooth muscle cells (HAVSMCs) to build an in vitro AS cell model. Moreover, miR-205-5p was silenced. Finally, cell viability was detected by MTT assay, cell apoptosis by flow cytometry and Western blot, and cell migration by the scratch test.
Results:
ICA could reduce lipid accumulation in the blood vessels of mice and plaque formation to treat AS. ICA promoted apoptosis and inhibited cell migration of HAVSMCs induced by ox-LDL. Moreover, cell proliferation and migration were inhibited via ICA, which was restored by miR-205-5p silencing.
Conclusion:
ICA can alleviate AS and inhibit the proliferation and migration of HAVSMCs induced by ox-LDL, potentially mediated by the upregulation of miR-205-5p.
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