Abstract
Abstract: :
Purpose: We recently demonstrated that Interleukin–10 (IL–10) inhibits the apoptosis of serum deprived retinal ganglion cells (RGCs). The purpose of this study was to investigate whether IL–10 mediated protection of RGCs is associated with the activation of nuclear factor–kB (NF–kB). Methods: Apoptosis in the rat retinal ganglion cell line (RGC–5) was induced by serum deprivation. The anti–apoptotic effect of IL–10 was studied by assaying the cellular viability using the formazan assay. Activation of NF–kB by IL–10 was assessed by studying the protective effect of IL–10 in the presence of cell–permeable NF–kB inhibitor peptide SN50. Results: Serum deprivation induced the apoptotic death in retinal ganglion cells. The viability of serum deprived retinal ganglion cells treated with IL–10 was 83% ± 1.1 (mean ± SEM, n = 8) after 48 h, whereas, only 55% ± 0.7 (mean ± SEM, n = 8) cells were viable without IL–10 treatment compared to serum complete control. The viability of serum deprived RGCs was reduced to 53% ± 0.4 (mean ± SEM, n = 8) in the presence of SN50 and IL–10, whereas inactive control peptide SN50M had no effect on the IL–10 mediated protection of serum deprived RGCs. Conclusions: The NF–kB inhibitor SN50 suppressed the IL–10 mediated protection of serum deprived RGCs. These results suggest that IL–10 may exert its neuroprotective effect in serum deprived RGCs by activating NF–kB which plays an important role in cell survival. Additional experiments are in progress to confirm these observations.
Keywords: apoptosis/cell death • neuroprotection • retinal culture