Abstract: Objective To study the effect of amyloid-beta (Aβ) on retinal ganglion cells (RGC) in mouse retina, and explore the role of p38MAPK pathway in this process. Methods Mice were randomly divided into three groups: experimental group, control group and intervention group. Seven days after intravitreal injection, the distribution pattern of Aβ on retina tissue was detected by immunofluorescence technique. RGC in retinal flatmount were stained by immunofluorescence and counted by quantitative analysis. In situ detection of cell apoptosis in RGC layer was performed by TUNEL assay. Active caspase-3 in RGC layer was detected by fluorescent immunohistochemical methods. Cellular morphology of RGC was observed using transmission electron microscope. The expression of p-p38MAPK in the retina was observed by Western blot. Results Seven days after intravitreal injection, Aβ was found immunofluorescent stained in all layers of retina tissue, with strong fluorescence signal in retinal neurepithelium layer and photoreceptor cell layer. In experimental group, the number of RGC was significantly decreased (P<0.05), while the number of TUNEL-positive or caspase-3 positive cells was significantly increased (P<0.05), compared with that in control group respectively. The classic morphologic characteristics of apoptosis were observed in RGC by transmission electron microscope. The expression of p38MAPK phosphorylation in retina was significantly increased. In intervention group, SB203580 obviously suppressed these changes on RGC induced by Aβ. Conclusions Aβ could induce apoptosis of retina ganglion cell, and p38MAPK signaling pathway may play an apoptosis-promoting role in this process.

Key words: Amyloid-beta, Retinal ganglion cells, Cell apoptosis, p38MAPK