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Granulocyte stimulating factor attenuates hypoxic-ischemic brain injury by inhibiting apoptosis in neonatal rats.

   
Author Bong Rim Kim, Jae Won Shim, Dong Kyung Sung, Sung Shin Kim, Ga Won Jeon, Myo Jing Kim, Yun Sil Chang, Won Soon Park, Eung Sang Choi
Citation Information Yonsei medical journal, 49:836-42 (2008)
Keywords Animals, Apoptosis, Brain, Cerebral Infarction, Flow Cytometry, Granulocyte Colony-Stimulating Factor, Hypoxia-Ischemia, Brain, In Situ Nick-End Labeling, Male, Organ Size, Protective Agents, Rats, Rats, Sprague-Dawley, Weight Gain
Related Products S7100
Pub Med ID 18972605
   

Abstract

[Full Text Article]
PURPOSE: This study was undertaken to determine the neuroprotective effect of granulocyte stimulating factor (G-CSF) on neonatal hypoxic-ischemic brain injury. MATERIALS AND METHODS: Seven-day-old male newborn rat pups were subjected to 110 minutes of 8% oxygen following a unilateral carotid artery ligation. Apoptosis was identified by performing terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining and flow cytometry with a combination of fluorescinated annexin V and propidium iodide (PI) and JC-1 (5,5',6,6'-tetrachloro-1,1',3,3'- tetraethylbenzimidazolyl-carbocyanine iodide). The extent of cerebral infarction was evaluated at 2 weeks after recovery. RESULTS: With a single dose (50microg/kg) of G-CSF treatment immediately after hypoxic-ischemic insult, hypoxia-ischemia induced increase in TUNEL-positive cells, annexinV+/PI- and JC-1 positive apoptotic cells in the ipsilateral cerebral cortex was significantly reduced at 24 hours, measured by flow cytometry, and the extent of cerebral infarction at 2 weeks after recovery was also significantly attenuated compared to the hypoxia-ischemia control group. CONCLUSION: Our data suggest that G-CSF is neuroprotective by inhibiting apoptosis, thereby reducing the ensuing cerebral infarction in a newborn rat pup model of cerebral hypoxia-ischemia (HI).