Icariin alleviates atherosclerosis by regulating the miR-205-5p/ERBB4/AKT signaling pathway

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 li-poprotein (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.

Automated summary

This study aims to investigate the effect and mechanism of icariin in treating atherosclerosis. It was found that icariin can reduce lipid accumulation and plaque formation, promoting apoptosis and inhibiting cell migration. The inhibitory effects on cell proliferation and migration by icariin were restored by silencing miR-205-5p.