scholarly journals Granulocyte-Colony Stimulating Factor Delays PWI/DWI Mismatch Evolution and Reduces Final Infarct Volume in Permanent-Suture and Embolic Focal Cerebral Ischemia Models in the Rat

Stroke ◽  
2009 ◽  
Vol 40 (9) ◽  
pp. 3102-3106 ◽  
Author(s):  
Bernt T. Bråtane ◽  
James Bouley ◽  
Armin Schneider ◽  
Birgul Bastan ◽  
Nils Henninger ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor

scholarly journals G-CSF Reduces Infarct Volume and Improves Functional Outcome after Transient Focal Cerebral Ischemia in Mice

2005 ◽  
Vol 25 (4) ◽  
pp. 431-439 ◽  
Author(s):  
Claire L Gibson ◽  
Philip MW Bath ◽  
Sean P Murphy
Keyword(s):  
Cerebral Ischemia ◽  
Water Maze ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Lesion Volume ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor

Growth factors possess neuroprotective and neurotrophic properties in vitro, but few have been extensively studied in vivo after stroke. In the present study, we investigated the potential functional benefits of granulocyte colony-stimulating factor (G-CSF) administration after focal cerebral ischemia. Male mice underwent 60-minute middle cerebral artery occlusion (MCAO) and received G-CSF (50 μg/kg, subcutaneously) or vehicle (saline) at the onset of reperfusion. Granulocyte colony-stimulating factor-treated mice killed at 48 hours after MCAO revealed a >45% reduction ( P<0.05) in lesion volume. In terms of body weight recovery, and in tests of motor (grid test and rotarod) and cognitive ability (water maze), MCAO significantly worsened the outcome in vehicle-treated mice as compared with shams ( P<0.05). However, G-CSF treatment was beneficial as, compared with vehicle, this significantly improved weight recovery and motor ability. This effect was most apparent on the water maze where G-CSF-treated mice were indistinguishable from shams in terms of acquiring the task. These results indicate long-term beneficial effects of a single dose of G-CSF administered on reperfusion, and illustrate the need to further investigate the mechanisms of G-CSF action.

scholarly journals Meta-Analysis of the Efficacy of Granulocyte-Colony Stimulating Factor in Animal Models of Focal Cerebral Ischemia

Stroke ◽  
2008 ◽  
Vol 39 (6) ◽  
pp. 1855-1861 ◽  
Author(s):  
Jens Minnerup ◽  
Jan Heidrich ◽  
Jürgen Wellmann ◽  
Andreas Rogalewski ◽  
Armin Schneider ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Animal Models ◽  
Focal Cerebral Ischemia ◽  
Meta Analysis ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor

Granulocyte colony-stimulating factor enhances angiogenesis after focal cerebral ischemia

2005 ◽  
Vol 1058 (1-2) ◽  
pp. 120-128 ◽  
Author(s):  
Soon-Tae Lee ◽  
Kon Chu ◽  
Keun-Hwa Jung ◽  
Song-Yi Ko ◽  
Eun-Hee Kim ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor

Abstract 42: Effects Of Intracerebroventricular Application Of Granulocyte Colony-stimulating Factor On Cerebral Recovery After Cardiac Arrest In Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Tobias Rabsahl ◽  
Erik Popp ◽  
Peter Vogel ◽  
Peter Teschendorf ◽  
Bernd W Boettiger
Keyword(s):  
Cardiac Arrest ◽  
Cerebral Ischemia ◽  
Histological Analysis ◽  
Neuronal Degeneration ◽  
Focal Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Single Shot ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor

Introduction: After transient global cerebral ischemia, selective vulnerable brain areas show delayed neuronal degeneration with characteristic signs of apoptosis. Recent data demonstrated potent neuroprotective effects of the application of granulocyte colony-stimulating factor (G-CSF) after focal cerebral ischemia. In order to assess possible effects of intracerebroventricular application of G-CSF on cerebral recovery after global cerebral ischemia due to cardiac arrest (CA) neurological testing according to a tape removal test as well as histological analysis of the hippocampal CA-1 sector were performed. Methods: Global cerebral ischemia was initiated by ventricular fibrillation in rats during general anesthesia. After 6 min of CA cardio pulmonary resuscitation (CPR) was initiated. After restoration of spontaneous circulation (ROSC) the animals were divided into two groups (G-CSF vs. placebo; n=16 per group). G-CSF (4μl=3.84μg) or placebo was applied in single shot technique 30 min after ROSC. During CA, CPR and for the first 24 h after ROSC all animals were kept normothermic using a feedback control system with intraperitoneal implanted telemetric probes. The tape removal test was applied pre-CA, 24 h, 3 d, 7 d, 10 d and 14 d after ROSC. After 14 days histological analysis was done by counting TUNEL positive neurons in the hippocampal CA-1 sector. All experiments were performed in a randomized and blinded setting. Results: All animals were kept normothermic within the first 24 h after ROSC (G-CSF: 37.3 ± 0.3 °C; placebo: 37.5 ± 0.5 °C). Pre-CA all animals removed the adhesive tapes promptly. After ROSC in both treatment groups a clear neurological damage was shown that improved within the first 14 days, without reaching baseline values. No statistically significant differences between the group could be seen. With regard to TUNEL-positive neurons in the hippocampal CA-1 sector no significant differences could be observed between the groups (G-CSF: 47 ± 22; placebo: 51 ± 24). Conclusions: Regarding neurological recovery and neurohistopathological outcome 14 d after global cerebral ischemia, the present study was not able to show any beneficial effects of G-CSF, despite the well known effects of G-CSF in non global cerebral ischemia models.

scholarly journals Neuroprotective Effect of Granulocyte Colony–Stimulating Factor After Focal Cerebral Ischemia

Stroke ◽  
2003 ◽  
Vol 34 (3) ◽  
pp. 745-751 ◽  
Author(s):  
W.-R. Schäbitz ◽  
R. Kollmar ◽  
M. Schwaninger ◽  
E. Juettler ◽  
J. Bardutzky ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Neuroprotective Effect ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor

scholarly journals Granulocyte-Colony Stimulating Factor Increases Cerebral Blood Flow via a NO Surge Mediated by Akt/eNOS Pathway to Reduce Ischemic Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Hock-Kean Liew ◽  
Jon-Son Kuo ◽  
Jia-Yi Wang ◽  
Cheng-Yoong Pang
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Infarct Volume ◽  
Neurological Deficits ◽  
No Production ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Regional Cerebral Blood ◽  
Rapid Reduction ◽  
Stimulating Factor

Granulocyte-colony stimulating factor (G-CSF) protects brain from ischemic/reperfusion (I/R) injury, and inhibition of nitric oxide (NO) synthases partially reduces G-CSF protection. We thus further investigated the effects of G-CSF on ischemia-induced NO production and its consequence on regional cerebral blood flow (rCBF) and neurological deficit. Endothelin-1 (ET-1) microinfused above middle cerebral artery caused a rapid reduction of rCBF (ischemia) which lasted for 30 minutes and was followed by a gradual recovery of blood flow (reperfusion) within the striatal region. Regional NO concentration increased rapidly (NO surge) during ischemia and recovered soon to the baseline. G-CSF increased rCBF resulting in shorter ischemic duration and an earlier onset of reperfusion. The enhancement of the ischemia-induced NO by G-CSF accompanied by elevation of phospho-Akt and phospho-eNOS was noted, suggesting an activation of Akt/eNOS. I/R-induced infarct volume and neurological deficits were also reduced by G-CSF treatment. Inhibition of NO synthesis by L-NG-Nitroarginine Methyl Ester (L-NAME) significantly reduced the effects of G-CSF on rCBF, NO surge, infarct volume, and neurological deficits. We conclude that G-CSF increases rCBF through a NO surge mediated by Akt/eNOS, which partially contributes to the beneficial effect of G-CSF on brain I/R injury.

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