Abstract
Purpose :
Inflammation is a known key player in the death of retinal pigment epithelium (RPE) cells and the development of age-related macular degeneration (AMD). Dysfunctional mitochondria, which release reactive oxygen species can be at the start of a detrimental inflammatory reaction. Here we assessed the effects of luteolin, a known anti-oxidant, on antimycin A (AMA)-induced mitochondria damage and inflammation in a human RPE cell line.
Methods :
Fully confluent ARPE-19 cells were exposed to AMA with or without a four-hour pretreatment with luteolin. Medium samples and cell lysates were collected and the release of inflammatory cytokines interleukin (IL)-6 and IL-8 was measured using ELISA. The effect of AMA on mitochondria was determined using transmission electron microscopy and mitoTRACKER staining. Cell death was determined using the MTT and LDH assays.
Results :
AMA induced severe swelling of mitochondria and cell death. Additionally, the release of the pro-inflammatory cytokine IL-6 was increased following AMA exposure. A pretreatment with luteolin prevented the release of pro-inflammatory cytokines, IL-6 and IL-8, but could not prevent cell death.
Conclusions :
Luteolin is an effective, anti-inflammatory agent in RPE cells suffering from severe mitochondrial dysfunction. Decreasing the release of pro-inflammatory cytokines from stressed RPE cells could potentially prevent the exacerbation of a chronic low-level inflammation of the RPE and slow the development of AMD.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.