An SPM-Enriched Marine Oil Supplement Shifted Microglia Polarization toward M2, Ameliorating Retinal Degeneration in rd10 Mice

Retinitis pigmentosa (RP) is the most common inherited retinal dystrophy causing progressive vision loss. It is accompanied by chronic and sustained inflammation, including M1 microglia activation. This study evaluated the effect of an essential fatty acid (EFA) supplement containing specialized pro...

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Published in:Antioxidants 2022-12, Vol.12 (1), p.98
Main Authors: Olivares-González, Lorena, Velasco, Sheyla, Gallego, Idoia, Esteban-Medina, Marina, Puras, Gustavo, Loucera, Carlos, Martínez-Romero, Alicia, Peña-Chilet, María, Pedraz, José Luis, Rodrigo, Regina
Format: Article
Language:English
Subjects:
Dietary supplements
Disease
Electroretinograms
Enzyme-linked immunosorbent assay
Enzymes
Fatty acids
Flow cytometry
Gene expression
Inflammation
inherited retinal dystrophies
Lipid peroxidation
Lipids
Lipopolysaccharides
Metabolites
Microglia
Oral administration
Oxidative stress
Phenotypes
Polarization
Retina
Retinal degeneration
Retinitis
Retinitis pigmentosa
specialized pro-resolving mediators
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Summary:Retinitis pigmentosa (RP) is the most common inherited retinal dystrophy causing progressive vision loss. It is accompanied by chronic and sustained inflammation, including M1 microglia activation. This study evaluated the effect of an essential fatty acid (EFA) supplement containing specialized pro-resolving mediators (SPMs), on retinal degeneration and microglia activation in mice, a model of RP, as well as on LPS-stimulated BV2 cells. The EFA supplement was orally administered to mice from postnatal day (P)9 to P18. At P18, the electrical activity of the retina was examined by electroretinography (ERG) and innate behavior in response to light were measured. Retinal degeneration was studied via histology including the TUNEL assay and microglia immunolabeling. Microglia polarization (M1/M2) was assessed by flow cytometry, qPCR, ELISA and histology. Redox status was analyzed by measuring antioxidant enzymes and markers of oxidative damage. Interestingly, the EFA supplement ameliorated retinal dysfunction and degeneration by improving ERG recording and sensitivity to light, and reducing photoreceptor cell loss. The EFA supplement reduced inflammation and microglia activation attenuating M1 markers as well as inducing a shift to the M2 phenotype in mouse retinas and LPS-stimulated BV2 cells. It also reduced oxidative stress markers of lipid peroxidation and carbonylation. These findings could open up new therapeutic opportunities based on resolving inflammation with oral supplementation with SPMs such as the EFA supplement.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox12010098