International immunopharmacology · 2022
Icariin alleviates atherosclerosis by regulating the miR-205-5p/ERBB4/AKT signaling pathway.
СтатьяНазвание и аннотация: Перевод в очереди
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Huang Peng, Wang Fengjun, Zhang Yibing, Zhang Yang, Qin Meng, Ji Jiahua, Wei Dexian, Ren Liqun
Аннотация
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.
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.