Previous studies have indicated that
NaIO3 induces intracellular
reactive oxygen species (ROS) production and has been used as a model for
age-related macular degeneration (AMD) due to the selective retinal pigment epithelium (RPE) cell damage it induces.
Beta-mangostin (BM) is a
xanthone-type natural compound isolated from Cratoxylum arborescens. The influence of BM on NaIO3-induced oxidative stress damage in ARPE-19 cells has not yet been elucidated. In this study, we investigated how BM protects ARPE-19 cells from NaIO3-induced ROS-mediated apoptosis. Our results revealed that BM notably improved cell viability and prevented ARPE-19 cell
mitochondrial dysfunction mediated-apoptosis induced by
NaIO3; it was mediated by significantly reduced NaIO3-upregulated ROS, cellular H2O2 production and improved downregulated
glutathione and
catalase activities. Furthermore, we found that BM could suppress the expression of Bax, cleaved PARP, and cleaved
caspase-3 by decreasing phosphorylation of
MEK/ERK and p53 expression in NaIO3-induced ARPE-19 cells. At the same time, we also used
MEK inhibitors (
PD98059) to confirm the above phenomenon. Moreover, our animal experiments revealed that BM prevented
NaIO3 from causing
retinal deformation; it led to thicker outer and inner nuclear layers and downregulated cleaved
caspase-3 expression compared to the group receiving
NaIO3 only. Collectively, these results suggest that BM can protect the RPE and retina from NaIO3-induced apoptosis through ROS-mediated
mitochondrial dysfunction involving the
MEK/ERK and p53 signaling pathways.