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Rong-Kung Tsai; Neuroprotective effects of recombinant human granulocyte colony-stimulationg factor (G-CSF) in a rat model of anterior ischemic optic neuropathy (rAION). Invest. Ophthalmol. Vis. Sci. 2013;54(15):1420.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the neuroprotective effects of granulocyte colony stimulationg factor (G-CSF) administration in a rat model of anterior ischemic optic neuropathy (rAION)
Using laser-induced photoactivation of intravenously administered rose Bengal in the right eyes of 48 adult male Wihistar rats. Rats were induced an anterior ischemic optic neuropathy . Rats are either immediately received G-CSF (subcutaneous injections, 100μg/Kg/day in 0.2 ml saline) or phosphated balanced saline (PBS) for 5 consecutive days. Rats are euthanized at 4 weeks post infarct. Density of retinal ganglion cells (RGCs) are counted using retrograde labeling of Fluoro-gold. Tunnel assay was conducted in the retinal sections and immunohistochemical staining of ED1 (marker of macrophage/microglia) was investigated in the optic nerve (ON) specimens.
The RGC densities in the central and mid-peripheral retinas in the G-CSF treated rats were significantly higher than those of the PBS-treated rats (survival rate was 71.4% vs. 33.2% in the central retina; 61.8% vs. 22.7% in mid-peripheral retina, respectively;p<0.05). TuNEL assays showed fewer apoptotic cells in the retinal ganglion cell layers of G-CSF treated rats (1.3±1.0/HPF vs. 8.0±1.5/HPF; p<0.001). In addition, the number of ED1 positive cells was attnuated at the optic nerve sections of G-CSF treated rats (16±6/HPF vs. 35±10/HPF; p=0.016).
Administration of G-CSF is neuroprotective in the rat model of anterior ischemic optic neuropathy. G-CSF may work via dual actions of anti-apoptosis for RGC surviving as well as anti-inflammation in the optic nerves as evidenced by less ED1-povitive cells infiltration.
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