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Maria Hytti, Eveliina Korhonen, Niina Piippo, Kai Kaarniranta, Anu Kauppinen; Luteolin decreases mitochondrial damage-associated inflammation in human retinal pigment epithelial cells. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5256.
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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.
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.
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.
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.
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