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• W2916417022 abstract "BACKGROUND:Autophagy is characterized by the degradation of cellular components in autophagosomes. It plays a significant role in cerebral ischemic injury and has a complex functional connection with apoptosis. The neurovascular unit (NVU) is a structural and functional unit of the nervous system presented as a therapeutic target of stroke. This study aimed to investigate the effect of autophagy induced by ischemic damage on NVUs. MATERIAL AND METHODS:SH-SY5Y cells, C6 cells, and rat brain microvascular endothelial cells were cultured with oxygen-glucose deprivation (OGD) exposure for different time durations, and 3-methyladenine (3-MA) was added as an autophagy inhibitor. In all 3 cell lines, lactate dehydrogenase (LDH) release was measured. Furthermore, apoptosis was detected using Annexin V-fluorescein isothiocyanate/propidium iodide labeling and immunofluorescence staining. Autophagosomes were observed through AO/MDC (acridine orange/monodansycadaverine) double staining. LC3-II expression levels were evaluated by western blot analysis. RESULTS:In the OGD groups of 3 cell lines, LDH leakage, and apoptotic rates were obviously increased. Remarkable increase in LC3-II expression was found in the OGD groups of SH-SY5Y cells and C6 cells. However, 3-MA decreased the LC3-II expression to varying degrees. CONCLUSIONS:OGD could induce the over-activation of autophagy and augment the apoptotic activity in neurons and glial cells of NVUs." @default.
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• W2916417022 date "2019-02-21" @default.
• W2916417022 modified "2023-09-28" @default.
• W2916417022 title "Autophagy Induced by Oxygen-Glucose Deprivation Mediates the Injury to the Neurovascular Unit" @default.
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• W2916417022 doi "https://doi.org/10.12659/msm.915123" @default.
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