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Wei-Ning Lin, Yao-Tseng Wen, Rong-Kung Tsai; Neuroprotective effect of astaxanthin in a rat model of anterior ischemic optic neuropathy. Invest. Ophthalmol. Vis. Sci. 2018;59(9):2498. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Astaxanthin (AST) is a strong antioxidant and anti-inflammatory agent. In this study, we aimed to investigate the neuroprotective effect of AST in a rat model of anterior ischemic optic neuropathy (rAION).
The adult male Wistar rats were administered AST 10mg/kg or AST 100mg/kg by daily gavage for 8 consecutive days, 7 days prior to rAION induction until the day of rAION induction, to evaluate the neuroprotective effect of AST. Phosphate buffered saline (PBS) was treated as the control group. Visual function was assessed by flash visual-evoked potentials (FVEPs) 4 weeks post-rAION induction. The survival rate and apoptosis of retinal ganglion cells (RGCs) were determined by fluoroGold retrograde labeling and TUNEL assay respectively. Inflammation of the optic nerve (ON) was detected by staining of ED1.
The P1-N2 amplitude of FVEP and the RGC densities were significantly higher in the two AST groups, compared with the control group (P < 0.05). The number of apoptotic cells in the RGC layer was significantly decreased in the AST-administered rats (P < 0.05) compared with that in the control group. Treatment with AST reduced the level of extrinsic macrophage infiltration at the ON, compared with that in the control group (P < 0.05). The protective effects of AST were dose-dependent, as significant difference was observed between AST 10mg/kg group and AST 100mg/kg group (P < 0.05).
Our findings in this study demonstrate that AST has neuroprotective effect in a rAION model. The administration of AST reduces both RGC death and macrophage infiltration at the ON, as well as preserving visual function.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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