Calycosin-7-O-β-D-glucoside Attenuates OGD/R-Induced Damage by Preventing Oxidative Stress and Neuronal Apoptosis via the SIRT1/FOXO1/PGC-1α Pathway in HT22 Cells
Copyright © 2019 Xiangli Yan et al.
| Veröffentlicht in: | Neural plasticity. - 1998. - 2019(2019) vom: 21., Seite 8798069 |
|---|---|
| 1. Verfasser: | |
| Weitere Verfasser: | , , , , |
| Format: | Online-Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2019
|
| Zugriff auf das übergeordnete Werk: | Neural plasticity |
| Schlagworte: | Journal Article Research Support, Non-U.S. Gov't Forkhead Box Protein O1 Foxo1 protein, mouse Glucosides Isoflavones Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Ppargc1a protein, mouse calycosin-7-O-beta-D-glucoside Sirt1 protein, mouse mehr... |
| Zusammenfassung: | Copyright © 2019 Xiangli Yan et al. Neuronal apoptosis induced by oxidative stress is a major pathological process that occurs after cerebral ischemia-reperfusion. Calycosin-7-O-β-D-glucoside (CG) is a representative component of isoflavones in Radix Astragali (RA). Previous studies have shown that CG has potential neuroprotective effects. However, whether CG alleviates neuronal apoptosis through antioxidant stress after ischemia-reperfusion remains unknown. To investigate the positive effects of CG on oxidative stress and apoptosis of neurons, we simulated the ischemia-reperfusion process in vitro using an immortalized hippocampal neuron cell line (HT22) and oxygen-glucose deprivation/reperfusion (OGD/R) model. CG significantly improved cell viability and reduced oxidative stress and neuronal apoptosis. In addition, CG treatment upregulated the expression of SIRT1, FOXO1, PGC-1α, and Bcl-2 and downregulated the expression of Bax. In summary, our findings indicate that CG alleviates OGD/R-induced damage via the SIRT1/FOXO1/PGC-1α signaling pathway. Thus, CG maybe a promising therapeutic candidate for brain injury associated with ischemic stroke |
|---|---|
| Beschreibung: | Date Completed 27.07.2020 Date Revised 27.07.2020 published: Electronic-eCollection Citation Status MEDLINE |
| ISSN: | 1687-5443 |
| DOI: | 10.1155/2019/8798069 |