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Annagrazia Adornetto, Giuseppe Pasquale Varano, Carlo Nucci, Maria Tiziana Corasaniti, Luigi Antonio Morrone, Giacinto Bagetta, Rossella Russo; Post-ischemic treatment with azithromycin prevents retinal ganglion cell death induced by ischemia/reperfusion injury in rat. Invest. Ophthalmol. Vis. Sci. 2017;58(8):2564.
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© ARVO (1962-2015); The Authors (2016-present)
Azithromycin is a widely used semi-synthetic macrolide antibiotic endowed with anti-inflammatory and immunomodulatory properties. Inflammation has been identified as an important component in the pathogenesis and progression of glaucoma and a potential target to achieve retinal neuroprotection. Here we studied the effect of azithromycin on retinal ganglion cell (RGC) degeneration induced by transient increase of intraocular pressure in rat.
Retinal ischemia was induced in adult rats by transient elevation of intraocular pressure. RGCs were retrogradely labeled by Fluorogold and survival was assessed following a single dose of azithromycin or vehicle given systemically at the end of the ischemia. Expression of death-associated proteins and ERK activation were studied by western blotting. Expression and activity of MMP-2 and -9 were analyzed by gelatin zymography.
Acute post-injury administration of azithromycin significantly prevented RGC death. This effect was accompanied by reduced calpains activity and prevention of Bad upregulation. The observed neuroprotection was associated with a significant inhibition of MMP-2/-9 gelatinolytic activity and ERK1/2 phosphorylation.
Azithromycin affords neuroprotection by modifying the inflammatory state of the retina following ischemia/reperfusion injury suggesting its potential repurposing for glaucoma treatment.
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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