Autophagy serves as a protective effect against inflammatory injury of oxidative stress in ARPE-19 cell

To test the effect of autophagy on inflammatory damage resulting from oxidative stress in adult retinal pigment epithelial cell line (ARPE-19).

ARPE-19 cells were pretreated with 200 and 600 µmol/L hydrogen peroxide (H₂O₂) at various time intervals. The changes of cell morphology, cell viability, reactive oxygen species (ROS) level, autophagic activity, and the inflammatory cytokines (TNFα, IL-6, and TGFβ) were measured at baseline and after treatment with autophagy inducer rapamycin (Rapa) and suppressor wortmannin (Wort) or shATG5.

The levels of ROS, cytokines (TNFα, IL-6, and TGFβ), and autophagic activity were significantly increased in ARPE-19 cells after pretreated with H₂O₂ (all P<0.05) and IL-10 was significantly decreased (P<0.05). By upregulating autophagy, Rapa significantly reduced oxidative stress-induced secretion of pro-inflammatory factors (TNFα and IL-6) and ROS (all P<0.05), yet elevated the production of TGFβ (P<0.05). In contrast, suppression of autophagy through Wort or ATG5 knockdown reduced cell viability, increased cell apoptotic rate, and exacerbated the generation of ROS and inflammatory cytokines (TNFα, IL-6, and TGFβ; all P<0.05).

Autophagy demonstrates a protective effect on ARPE-19 cell through mitigating oxidative damage and oxidative stress-induced inflammatory response. Regulation of autophagy may be a potential way for age-related macular degeneration.