Brain-derived neurotrophic factor reduces cortical cell death by ischemia after middle cerebral artery occlusion in the rat

2001 ◽  
Vol 101 (3) ◽  
pp. 229-238 ◽  
Author(s):  
I. Ferrer ◽  
J. Krupinski ◽  
E. Goutan ◽  
E. Martí ◽  
S. Ambrosio ◽  
...  
Keyword(s):  
Cell Death ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neurotrophic Factor ◽  
Cortical Cell ◽  
Brain Derived Neurotrophic Factor ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion

Acupuncture attenuates neuronal cell death in middle cerebral artery occlusion model of focal ischemia

2010 ◽  
Vol 32 (sup1) ◽  
pp. 84-87 ◽  
Author(s):  
Kyoung Ah Kang ◽  
Eun Sim Shin ◽  
Jinyoung Hur ◽  
Mohmmad Rakibul Hasan ◽  
Hyejung Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Focal Ischemia ◽  
Artery Occlusion ◽  
Occlusion Model ◽  
Cerebral Artery Occlusion

scholarly journals Normobaric Hyperoxia Delays Perfusion/Diffusion Mismatch Evolution, Reduces Infarct Volume, and Differentially Affects Neuronal Cell Death Pathways after Suture Middle Cerebral Artery Occlusion in Rats

2007 ◽  
Vol 27 (9) ◽  
pp. 1632-1642 ◽  
Author(s):  
Nils Henninger ◽  
James Bouley ◽  
Julia M Nelligan ◽  
Kenneth M Sicard ◽  
Marc Fisher
Keyword(s):  
Cell Death ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Time Window ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Normobaric Hyperoxia ◽  
Cell Death Pathways ◽  
Cerebral Artery Occlusion

Normobaric hyperoxia (NBO) has been shown to extend the reperfusion window after focal cerebral ischemia. Employing diffusion (DWI)- and perfusion (PWI)-weighted magnetic resonance imaging (MRI), the effect of NBO (100% started at 30 mins after middle cerebral artery occlusion (MCAO)) on the spatiotemporal evolution of ischemia during and after permanent (pMCAO) and transient suture middle cerebral artery occlusion (tMCAO) was investigated (experiment 3). In two additional experiments, time window (experiment 1) and cell death pathways (experiment 2) were investigated in the pMCAO model. In experiment 1, NBO treatment reduced infarct volume at 24 h after pMCAO by 10% when administered for 3 h ( P > 0.05) and by 44% when administered for 6 h ( P < 0.05). In experiment 2, NBO acutely (390 mins, P < 0.05) reduced in situ end labeling (ISEL) positivity in the ipsilesional penumbra but increased contralesional necrotic as well as caspase-3-mediated apoptotic cell death. In experiment 3, CBF characteristics and CBF-derived lesion volumes did not differ between treated and untreated animals, whereas the apparent diffusion coefficient (ADC)-derived lesion volume essentially stopped progressing during NBO treatment, resulting in a persistent PWI/DWI mismatch that could be salvaged by delayed (3 h) reperfusion. In conclusion, NBO (1) acutely preserved the perfusion/diffusion mismatch without altering CBF, (2) significantly extended the time window for reperfusion, (3) induced lasting neuroprotection in permanent ischemia, and (4) although capable of reducing cell death in hypoperfused tissue it also induced cell death in otherwise unaffected areas. Our data suggest that NBO may represent a promising strategy for acute stroke treatment.

The NF-κB inhibitor diethyldithiocarbamate (DDTC) increases brain cell death in a transient middle cerebral artery occlusion model of ischemia

2001 ◽  
Vol 55 (3) ◽  
pp. 375-386 ◽  
Author(s):  
William D. Hill ◽  
David C. Hess ◽  
James E. Carroll ◽  
Chandramohan G. Wakade ◽  
Eugene F. Howard ◽  
...  
Keyword(s):  
Cell Death ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Brain Cell ◽  
Occlusion Model ◽  
Cerebral Artery Occlusion
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