Purpose: To investigate effects of intravitreal injections of triamcinolone acetonide (IVI-TA) at different times in a rodent model of nonarteritic anterior ischemic optic neuropathy (rAION).
Methods: After inducing ischemic optic neuropathy, the rats received either IVI-TA (0.32 mg/2 μL) at 1 day (1d-TA), 1 week (7d-TA), 2 weeks (14d-TA), or PBS. The density of retinal ganglion cells (RGCs) was calculated using retrograde Fluorogold labeling. Electrophysiological visual function was assessed by flash visual evoked potentials (FVEPs). Apoptosis assays of the retinal sections and immunohistochemistry of ED1 staining of the optic nerves were performed.
Results: Four weeks postinfarct, the 1d- and 7d-TA groups had significantly rescued RGCs in the central (2160 ± 250 mm(2), P = 0.004; 2050 ± 660, P = 0.008, respectively) and midperipheral retinas (1240 ± 130; 1250 ± 220, respectively, both P = 0.004) compared with those of the PBS-treated rats. Flash visual evoked potentials demonstrated improvements in P1 amplitude (μV) in the 1d- and 7d-TA groups (both P < 0.05). Assays of TUNEL showed a decrease in the number of apoptotic cells in the RGC layers of 1d- and 7d-TA-treated retinas compared with the PBS-treated group (both P = 0.004). Cells ED1-positive were significantly decreased in the optic nerve (ON) of the 1d- and 7d-TA groups compared with the PBS group (P = 0.004 and 0.02, respectively).
Conclusions: Within 1 week postinfarct of rAION, IVI-TA had neuroprotective effects on RGC survival with an increase in the electrophysiological amplitude of VEPs and a decrease in microglial infiltration in the ONs.