Abstract
Purpose:
We reported the effect of caspase3 siRNA on the retinal ganglion cell (RGC) damage induced by transient ischemic injury at 2009 ARVO meeting. We assumed that the effects of caspase3 siRNA lasted for a few days because of a long ischemic time or short period of siRNA breakdown. Therefore we investigated the effect of caspase3 siRNA on transient ischemic injury with a shorter ischemic time.
Methods:
even week-old male Wister rats were used. IOP was kept at 110mmHg for 60 60min or 120min, then brought back to normal. Caspase3 siRNA were injected into the vitreous cavity 24hr prior to transient ischemic injury. RGCs were labeled with Fluoro-Gold retrogradely at 3 days before the injury. Two or 7 days after the injury, flat-mounts of the retina were examined by fluorescence microscopy.
Results:
In 60min group, the numbers of RGCs were 1012.9(+/-87.3) /mm2 at 2days and 959.0(+/-87.3) /mm2 at 7days after the injury. In 120min group, the numbers were 839.5(+/-14.7) /mm2 at 2 days and 596.1(+/-99.6) /mm2 at 7 days after the injury. The number of RGCs at 7 days in 120 min group after the injury was decreased significantly (Mann-Whitney U-test: p<0.05).
Conclusions:
The neuroptotective effect of caspase3 siRNA could keep against mild ischemic injury. The effect may be maintained ffor longer time than we expected.
Keywords: 615 neuroprotection •
691 retina: proximal (bipolar, amacrine, and ganglion cells)