Scutellarin protects human retinal pigment epithelial cells against hydrogen peroxide (H₂O₂)-induced oxidative damage

Proliferative vitreoretinopathy (PVR) is a severe blinding complication of retinal detachment surgery. Increasing evidence demonstrate that PVR is associated with oxidative stress. Scutellarin is a natural flavone compound that has been reported to have anti-oxidative activity. However, the effect of scutellarin on PVR remains unknown. In the current study, we assessed the effect of scutellarin on hydrogen peroxide (H₂O₂)-induced oxidative injury in human retinal pigment epithelium cells (ARPE-19).

ARPE-19 cells were pretreated with different concentrations of scutellarin for 2 h, and then challenged with H₂O₂ (1 mM) for 24 h. The levels of reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) and glutathione (GSH) activity were measured to assess the level of oxidative stress. Flow cytometry was performed to detect the apoptosis rate of ARPE-19 cells. Expression levels of bcl-2, bax, cleaved-caspase-3, p-JAK2, JAK2, p-STAT3, and STAT3 were measured using western blot.

Our results revealed that scutellarin improved the cell viability of H₂O₂-induced ARPE-19 cells. Scutellarin alleviated the H₂O₂-induced oxidative stress in ARPE-19 cells, which was illustrated by reduced levels of ROS and MDA, accompanied by increased SOD activity and GSH level. The increased apoptosis rate of ARPE-19 cells caused by H₂O₂ induction was significantly decreased after scutellarin treatment. H₂O₂ treatment resulted in significant increase in bax expression and decrease in bcl-2 expression, while the changes in the expressions of bax and bcl-2 were reversed by scutellarin treatment. In addition, scutellarin promoted the activation of JAK2/STAT3 signaling pathway in H₂O₂-induced ARPE-19 cells. Suppression of JAK2/STAT3 signaling pathway abolished the protective effects of scutellarin on H₂O₂-induced ARPE-19 cells.

These findings suggested that scutellarin was capable for alleviating H₂O₂-induced oxidative damage in ARPE-19 cells, which might be ascribed to the activation of JAK2/STAT3 signaling pathway.