Thymoquinone protects human retinal pigment epithelial cells against hydrogen peroxide induced oxidative stress and apoptosis.

Oxidative stress in retinal pigment epithelium (RPE) cells may contribute to the progression of age-related macular degeneration. Thymoquinone (TQ), an active component derived from Nigella sativa, possesses antioxidative effect. However, the role of TQ in RPE cells under oxidative stress condition remains unclear. The present study aimed to examine the protective effect of TQ against hydrogen peroxide (H O )-induced oxidative stress in human RPE cells. Our results showed that TQ improved the cell viability and apoptosis in H O -induced ARPE cells. We also found that the levels of reactive oxygen species and malondialdehyde induced by H O were reduced after the pretreatment of TQ. In addition, the inhibitory effect of H O on the glutathione (GSH) level and superoxide dismutase activity was markedly attenuated by TQ pretreatment. Moreover, TQ enhanced the activation of Nrf2/heme oxygenase 1 (HO-1) signaling pathway in H O -induced ARPE cells. Knockdown of Nrf2 abolished the protective effect of TQ on H O -induced oxidative damage. These results suggested that TQ protected ARPE cells from H O -induced oxidative stress and apoptosis via the Nrf2/HO-1 signaling pathway.