S-(–)-equol alleviates stenosis of the injured carotid artery in Sprague Dawley rats by preventing the vascular smooth muscle cell phenotypic switch via inhibition of the MAPKp38-NFκBp65 signaling
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Published:2020-08-01
Issue:8
Volume:10
Page:1237-1248
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ISSN:2158-5849
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Container-title:Materials Express
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language:en
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Short-container-title:mat express
Author:
Wu Hongchen,Nie Piming,Zhou Zhenghua,Hu Jun,Li Guangjian,Zhang Mengjie,Tian Zhiqiang,Yang Xia,Ni Bing,Chen Kangning
Abstract
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.
Publisher
American Scientific Publishers
Subject
General Materials Science
Cited by
1 articles.
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