| Autor: |
Jun Hu, Zhiqiang Tian, Guangjian Li, Hongchen Wu, Piming Nie, Bing Ni, Kangning Chen, Mengjie Zhang, Xia Yang, Zheng-Hua Zhou |
| Rok vydání: |
2020 |
| Předmět: |
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| Zdroj: |
Materials Express. 10:1237-1248 |
| ISSN: |
2158-5849 |
| Popis: |
Phenotypic switching of the vascular smooth muscle cells (VSMCs) is closely related to an in-stent restenosis (ISR). This study aimed to investigate whether S-(–)-equol prevented the phenotypic switch of the VSMCs as a potential treatment of an ISR. The carotid arteries of female Sprague Dawley (SD) rats with or without a carotid injury and ovariectomy were harvested after 4 weeks of treatment with S-(–)-equol. Stenosis of the carotid artery and two phenotype-related proteins-α smooth muscle actin (αSMA) and osteopontin (OPN)-were determined. The proliferation and migration capacities of VSMCs were determined by the CCK-8 and transwell assays, respectively. The expressions of αSMA, OPN, MAPKp38, p-MAPKp38, NF-κBp65, and p-NF-κBp65 were detected by a western blot. S-(–)-equol alleviated carotid stenosis and prevented the VSMC phenotypic switch in female SD rats with a carotid artery injury and a bilateral ovariectomy. S-(–)-equol inhibited the phenotypic switch of VSMCs, which was induced by PDGF-BB, and enhanced the proliferation and migration of VSMCs. The effects of S-(–)-equol on VSMCs were confirmed to be related to the inactivation of the GPER-MAPKp38-NF-κBp65 signaling in vitro and in vivo. Our results indicate that S-(–)-equol affects carotid stenosis by preventing the phenotypic switch of VSMCs via the GPER-MAPKp38-NF-κBp65 signaling pathway. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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