The antioxidant effects of riluzole on the APRE-19 celll model injury-induced by t-BHP

Age-related macular degeneration (AMD) causes the dysfunction of the retinal pigment epithelial (RPE) cells. In this study, we examined the effects of riluzole, a sustained activator of the TRAAK potassium channel, on human RPE (ARPE-19) cells in an oxidant-induced cell-injury model and elucidate the mechanism of riluzole on RPE cell apoptosis.

These results demonstrate that riluzole protects RPE cells from apoptosis. The protection mechanism of riluzole could be from stabilizing mitochondrial Δψm and preventing the release of Cyt-c. Changes in TRAAK expression might also contribute to the protection of RPE cells.

The follow four groups of ARPE-19 cells were treated with riluzole and/or tert-butyl hydroperoxide (t-BHP) for 24.0 h: control, t-BHP, riluzole, and t-BHP + riluzole. Cell apoptosis was measured by flow cytometry, and Western blotting was performed to analyze the expression of the weakly inward rectifying potassium (TRAAK) channel. Finally, the mitochondrial membrane potential (Δψm) was detected by flow cytometry, and cytochrome C (Cyt-c) release was assessed by Western blotting.

The viability of the cells in the cotreated group was significantly higher (85.6 ± 3.1%) than that in the t-BHP group (66.2 ± 2.5%). In addition, the cells in the cotreated group had a higher effect on increasing the expression of TRAAK than the t-BHP group. The results also showed that Cyt-c translocation significantly decreased and Δψm increased in the cotreated group. Conclusions: These results demonstrate that riluzole protects RPE cells from apoptosis. The protection mechanism of riluzole could be from stabilizing mitochondrial Δψm and preventing the release of Cyt-c. Changes in TRAAK expression might also contribute to the protection of RPE cells.