Giuseppe Rovere1, Francisco M Nadal-Nicolás2, Paloma Sobrado-Calvo2, David García-Bernal3, Maria Paz Villegas-Pérez2, Manuel Vidal-Sanz2, Marta Agudo-Barriuso2. 1. Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia e Instituto Murciano de Investigación Biosanitaria-Hospital Universitario Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain 2Faculty of Medicine, Tor Vergata University, Rome, Italy. 2. Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia e Instituto Murciano de Investigación Biosanitaria-Hospital Universitario Virgen de la Arrixaca (IMIB-Arrixaca), Murcia, Spain. 3. Terapia celular y trasplante hematopoyético (IMIB-Arrixaca), Murcia, Spain.
Abstract
PURPOSE: To study the effect of topical administration of bromfenac, a nonsteroidal anti-inflammatory drug (NSAID), on retinal gliosis and levels of prostaglandin E2 (PGE2) after complete optic nerve crush (ONC). METHODS: Adult albino rats were divided into the following groups (n = 8 retinas/group): (1) intact, (2) intact and bromfenac treatment (twice a day during 7 days), (3) ONC (7 days), and (4) ONC (7 days) + bromfenac treatment (twice a day during 7 days). Animals from groups 3 and 4 were imaged in vivo with spectral-domain optical coherence tomography (SD-OCT) before the procedure and 15 minutes, 3, 5, or 7 days later. Retinas from all groups were analyzed by immunodetection, Western blotting, or enzyme-linked immunoabsorbent assay (ELISA). RESULTS: Quantification of Brn3a (brain-specific homeobox/POU domain protein 3A) +RGCs (retinal ganglion cells) in cross sections showed that bromfenac treatment does not accelerate ONC-induced degeneration. Cellular retinaldehyde binding protein 1 regulation indicated that bromfenac improves retinal homeostasis in injured retinas. Spectral-domain OCT showed that the thickness of the retina and the retinal nerve fiber layer at 7 days post ONC was significantly reduced in bromfenac-treated animals when compared to untreated animals. In agreement with these data, hypertrophy of astrocytes and Müller cells and expression of glial fibrillary acidic protein and vimentin were greatly diminished by bromfenac treatment. While no changes in cyclooxygenase (COX) enzyme COX1 and COX2 expression were observed, there was a significant increase of PGE2 after ONC that was controlled by bromfenac treatment. CONCLUSIONS: Topical administration of bromfenac is an efficient and noninvasive treatment to control the retinal gliosis and release of proinflammatory mediators that follow a massive insult to the RGC population.
PURPOSE: To study the effect of topical administration of bromfenac, a nonsteroidal anti-inflammatory drug (NSAID), on retinal gliosis and levels of prostaglandin E2 (PGE2) after complete optic nerve crush (ONC). METHODS: Adult albino rats were divided into the following groups (n = 8 retinas/group): (1) intact, (2) intact and bromfenac treatment (twice a day during 7 days), (3) ONC (7 days), and (4) ONC (7 days) + bromfenac treatment (twice a day during 7 days). Animals from groups 3 and 4 were imaged in vivo with spectral-domain optical coherence tomography (SD-OCT) before the procedure and 15 minutes, 3, 5, or 7 days later. Retinas from all groups were analyzed by immunodetection, Western blotting, or enzyme-linked immunoabsorbent assay (ELISA). RESULTS: Quantification of Brn3a (brain-specific homeobox/POU domain protein 3A) +RGCs (retinal ganglion cells) in cross sections showed that bromfenac treatment does not accelerate ONC-induced degeneration. Cellular retinaldehyde binding protein 1 regulation indicated that bromfenac improves retinal homeostasis in injured retinas. Spectral-domain OCT showed that the thickness of the retina and the retinal nerve fiber layer at 7 days post ONC was significantly reduced in bromfenac-treated animals when compared to untreated animals. In agreement with these data, hypertrophy of astrocytes and Müller cells and expression of glial fibrillary acidic protein and vimentin were greatly diminished by bromfenac treatment. While no changes in cyclooxygenase (COX) enzyme COX1 and COX2 expression were observed, there was a significant increase of PGE2 after ONC that was controlled by bromfenac treatment. CONCLUSIONS: Topical administration of bromfenac is an efficient and noninvasive treatment to control the retinal gliosis and release of proinflammatory mediators that follow a massive insult to the RGC population.
Authors: Manuel Vidal-Sanz; Caridad Galindo-Romero; Francisco J Valiente-Soriano; Francisco M Nadal-Nicolás; Arturo Ortin-Martinez; Giuseppe Rovere; Manuel Salinas-Navarro; Fernando Lucas-Ruiz; Maria C Sanchez-Migallon; Paloma Sobrado-Calvo; Marcelino Aviles-Trigueros; María P Villegas-Pérez; Marta Agudo-Barriuso Journal: Front Neurosci Date: 2017-04-26 Impact factor: 4.677
Authors: Jose E Millán-Rivero; Francisco M Nadal-Nicolás; David García-Bernal; Paloma Sobrado-Calvo; Miguel Blanquer; Jose M Moraleda; Manuel Vidal-Sanz; Marta Agudo-Barriuso Journal: Sci Rep Date: 2018-11-02 Impact factor: 4.379