دورية أكاديمية
β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A
| العنوان: | β-asarone induces viability and angiogenesis and suppresses apoptosis of human vascular endothelial cells after ischemic stroke by upregulating vascular endothelial growth factor A |
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| المؤلفون: | Dazhong Sun, Lulu Wu, Siyuan Lan, Xiangfeng Chi, Zhibing Wu |
| المصدر: | PeerJ, Vol 12, p e17534 (2024) |
| بيانات النشر: | PeerJ Inc., 2024. |
| سنة النشر: | 2024 |
| المجموعة: | LCC:Medicine LCC:Biology (General) |
| مصطلحات موضوعية: | β-asarone, Ischemic stroke, Vascular endothelial growth factor A, Angiogenesis, Apoptosis, Medicine, Biology (General), QH301-705.5 |
| الوصف: | Ischemic stroke (IS) is a disease with a high mortality and disability rate worldwide, and its incidence is increasing per year. Angiogenesis after IS improves blood supply to ischemic areas, accelerating neurological recovery. β-asarone has been reported to exhibit a significant protective effect against hypoxia injury. The ability of β-asarone to improve IS injury by inducing angiogenesis has not been distinctly clarified. The experimental rats were induced with middle cerebral artery occlusion (MCAO), and oxygen-glucose deprivation (OGD) model cells were constructed using human microvascular endothelial cell line (HMEC-1) cells. Cerebral infarction and pathological damage were first determined via triphenyl tetrazolium chloride (TTC) and hematoxylin and eosin (H&E) staining. Then, cell viability, apoptosis, and angiogenesis were assessed by utilizing cell counting kit-8 (CCK-8), flow cytometry, spheroid-based angiogenesis, and tube formation assays in OGD HMEC-1 cells. Besides, angiogenesis and other related proteins were identified with western blot. The study confirms that β-asarone, like nimodipine, can ameliorate cerebral infarction and pathological damage. β-asarone can also upregulate vascular endothelial growth factor A (VEGFA) and endothelial nitric oxide synthase (eNOS) and induce phosphorylation of p38. Besides, the study proves that β-asarone can protect against IS injury by increasing the expression of VEGFA. In vitro experiments affirmed that β-asarone can induce viability and suppress apoptosis in OGD-mediated HMEC-1 cells and promote angiogenesis of OGD HMEC-1 cells by upregulating VEGFA. This establishes the potential for β-asarone to be a latent drug for IS therapy. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2167-8359 |
| Relation: | https://peerj.com/articles/17534.pdf; https://peerj.com/articles/17534/; https://doaj.org/toc/2167-8359 |
| DOI: | 10.7717/peerj.17534 |
| URL الوصول: | https://doaj.org/article/27c6f6e806594880be3239c6285b3aa3 |
| رقم الأكسشن: | edsdoj.27c6f6e806594880be3239c6285b3aa3 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 21678359 |
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| DOI: | 10.7717/peerj.17534 |