| ObjectiveTo investigate the effects of inhibition of the protein kinase CK2 on retinal ganglion cells of rats subjected to ischemia reperfusion injuryMethodsAn ischemia reperfusion model characterized by cannulation of the anterior chamber with elevated saline container was established for 75 minutes. A total number of 60 young adult (8-10weeks) Sprague-Dawley (SD) rats were used in this study. To study the time-course of RGC death induced by ischemia reperfusion, the numbers of RGCs were examined at 1 week,2weeks and 3weeks post-ischemia/reperfusion respectively. Rats in negative control group and positive control C group received three times of intravitreal injection of DMSO or TBB respectively, each of 3μl on days the 3rd,9th,15th, after ischemia/reperfusion. Fluorogold was used to retrogradely label surviving RGCs. The numbers of viable RGCs were assessed on the retinal whole-mounts 21 days after ischemia/reperfusion.ResultsSignificant amount of RGCs were lost at 2 and 3 weeks after ischemia/reperfusion, and the average numbers (±S.D.) of survival RGC were 1376±123 per mm2 in 3weeks after he ischemia/reperfusion group compared with the 2626±220 per mm2 in the control group (P<0.001). The average numbers (±S.D.) of surviving RGCs after injection of DMSO and TBB (2.5mM) were 1282±15 per mm2 and 1865±171 per mm2. There was a significant difference between the TBB group and the positive control C group.Conclusion1. RGCs loss was induced after ischemia/reperfusion, especially after 2 and 3 weeks post ischemia reperfusion injury.2. The inhibition of CK2 via intravitreal injection of CK2 inhibitor TBB resulted in protection of RGC. Results of our study provided an impetus for investigation of the mechanism of RGC survival mediated by CK2 inhibition.
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