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

BACKGROUND

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 (HO)-induced oxidative injury in human retinal pigment epithelium cells (ARPE-19).

METHODS

ARPE-19 cells were pretreated with different concentrations of scutellarin for 2 h, and then challenged with HO (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.

RESULTS

Our results revealed that scutellarin improved the cell viability of HO-induced ARPE-19 cells. Scutellarin alleviated the HO-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 HO induction was significantly decreased after scutellarin treatment. HO 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 HO-induced ARPE-19 cells. Suppression of JAK2/STAT3 signaling pathway abolished the protective effects of scutellarin on HO-induced ARPE-19 cells.

CONCLUSION

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