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