June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Luteolin decreases mitochondrial damage-associated inflammation in human retinal pigment epithelial cells
Author Affiliations & Notes
  • Maria Hytti
    University of Eastern Finland, Kuopio, Finland
  • Eveliina Korhonen
    University of Eastern Finland, Kuopio, Finland
  • Niina Piippo
    University of Eastern Finland, Kuopio, Finland
  • Kai Kaarniranta
    University of Eastern Finland, Kuopio, Finland
    Kuopio University Hospital, Kuopio, Finland
  • Anu Kauppinen
    University of Eastern Finland, Kuopio, Finland
  • Footnotes
    Commercial Relationships   Maria Hytti, None; Eveliina Korhonen, None; Niina Piippo, None; Kai Kaarniranta, None; Anu Kauppinen, None
  • Footnotes
    Support  Finnish Cultural Foundation - North-Savo Regional Fund
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 5256. doi:
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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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      © ARVO (1962-2015); The Authors (2016-present)

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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.

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