scholarly journals Magnolol protects against ischemic-reperfusion brain damage following oxygen-glucose deprivation and transient focal cerebral ischemia

2018 ◽  
Author(s):  
Sheng‑Yang Huang ◽  
Shih‑Huang Tai ◽  
Che‑Chao Chang ◽  
Yi‑Fang Tu ◽  
Chih‑Han Chang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Focal Cerebral Ischemia ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Ischemic Reperfusion ◽  
Transient Focal Cerebral Ischemia

The effect of oxygen therapy on brain damage and cerebral pO2in transient focal cerebral ischemia in the rat

2007 ◽  
Vol 28 (8) ◽  
pp. 963-976 ◽  
Author(s):  
Huagang Hou ◽  
Oleg Grinberg ◽  
Benjamin Williams ◽  
Stalina Grinberg ◽  
Hongsheng Yu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Oxygen Therapy ◽  
Focal Cerebral Ischemia ◽  
Transient Focal Cerebral Ischemia ◽  
Effect Of Oxygen

scholarly journals EphrinB2-EphB2 signaling for dendrite protection after neuronal ischemia in vivo and oxygen-glucose deprivation in vitro

2020 ◽  
pp. 0271678X2097311
Author(s):  
Zhanyang Yu ◽  
Wenlu Li ◽  
Jing Lan ◽  
Kazuhide Hayakawa ◽  
Xunming Ji ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Mouse Model ◽  
Therapeutic Potential ◽  
Focal Cerebral Ischemia ◽  
Ischemic Injury ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Neuron Soma

In order to rescue neuronal function, neuroprotection should be required not only for the neuron soma but also the dendrites. Here, we propose the hypothesis that ephrin-B2-EphB2 signaling may be involved in dendritic degeneration after ischemic injury. A mouse model of focal cerebral ischemia with middle cerebral artery occlusion (MCAO) method was used for EphB2 signaling test in vivo. Primary cortical neuron culture and oxygen-glucose deprivation were used to assess EphB2 signaling in vitro. siRNA and soluble ephrin-B2 ectodomain were used to block ephrin-B2-Ephb2 signaling. In the mouse model of focal cerebral ischemia and in neurons subjected to oxygen-glucose deprivation, clustering of ephrin-B2 with its receptor EphB2 was detected. Phosphorylation of EphB2 suggested activation of this signaling pathway. RNA silencing of EphB2 prevented neuronal death and preserved dendritic length. To assess therapeutic potential, we compared the soluble EphB2 ectodomain with the NMDA antagonist MK801 in neurons after oxygen-glucose deprivation. Both agents equally reduced lactate dehydrogenase release as a general marker of neurotoxicity. However, only soluble EphB2 ectodomain protected the dendrites. These findings provide a proof of concept that ephrin-B2-EphB2 signaling may represent a novel therapeutic target to protect both the neuron soma as well as dendrites against ischemic injury.

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