1,721,005 research outputs found
Saffron supplement maintains morphology and function after exposure to damaging light in mammalian retina
PURPOSE:
To test whether the saffron extract (Crocus sativus L.) given as a dietary supplement counteracts the effects of continuous light exposure in the albino rat retina.
METHODS:
Three experimental groups of Sprague-Dawley rats were used. Experimental animals were prefed either saffron or beta-carotene (1 mg extract/kg/d) before they were exposed to bright continuous light (BCL) for 24 hours. Flash electroretinograms (fERGs) were recorded in control and treated rats the day before and 1 week after light exposure. At the end of the second recording session, the animals were killed and the retinas were quickly removed, fixed, cryosectioned, and labeled so that the thickness of the outer nuclear layer (ONL) could be analyzed. Changes in protein level and cellular localization of fibroblast growth factor (FGF)2 were determined by Western blot analysis and retinal immunohistochemistry, respectively. In a second series of experiments, rats were killed at the end of light exposure, and the amount of apoptotic figures in the ONL was assessed by terminal transferase-mediated deoxyuridine triphosphate (d-UTP)-biotin nick-end labeling (TUNEL). BCL induced DNA fragmentation, characteristic of dying cells, almost exclusively in the photoreceptor layer. The rate of photoreceptor death induced by BCL is expressed as the frequency of TUNEL-positive profiles per millimeter.
RESULTS:
The photoreceptor layer was largely preserved in saffron-treated animals because it was the fERG response. In addition, the rate of photoreceptor death induced by BCL appeared drastically reduced in treated animals. In beta-carotene prefeeding experiments, morphologic analysis showed preservation of the ONL similar to that obtained with saffron prefeeding, whereas the fERG response was unrecordable. Western blot analysis showed that exposure to light induced a strong upregulation of FGF2 in control and beta-carotene-treated rats, but s no change was noted in saffron-treated rats.
CONCLUSIONS:
These results show that saffron may protect photoreceptors from retinal stress, maintaining both morphology and function and probably acting as a regulator of programmed cell death
The impact of organic inhibitors of the hyperpolarization activated current (Ih) on the electroretinogram (ERG) of rodents
Up-regulation of pro-angiogenic pathways and induction of neovascularization by an acute retinal light damage.
The light damage (LD) model was mainly used to study some of the main aspects of age related macular degeneration (AMD), such as oxidative stress and photoreceptor death. Several protocols of light-induced retinal degeneration exist. Acute light damage is characterized by a brief exposure (24 hours) to high intensity light (1000 lux) and leads to focal degeneration of the retina which progresses over time. To date there are not experimental data that relate this model to neovascular events. Therefore, the purpose of this study was to characterize the retina after an acute light damage to assess whether the vascularization was affected. Functional, molecular and morphological investigations were carried out. The electroretinographic response was assessed at all recovery times (7, 60, 120 days after LD). Starting from 7 days after light damage there was a significant decrease in the functional response, which remained low up to 120 days of recovery. At 7 days after light exposure, neo-vessels invaded the photoreceptor layer and retinal neovascularization occurred. Remarkably, neoangiogenesis was associated to the up-regulation of VEGF, bFGF and their respective receptors (VEGFR2 and FGFR1) with the progression of degeneration. These important results indicate that a brief exposure to bright light induces the up-regulation of pro-angiogenic pathways with subsequent neovascularization
Cerium oxide nanoparticles reduce the accumulation of autofluorescent deposits in light-induced retinal degeneration: Insights for age-related macular degeneration
Ophthalmic Applications of Cerium Oxide Nanoparticles
Cerium oxide nanoparticles (CeO2-NPs; or nanoceria) have been largely studied for biomedical applications due to their peculiar auto-regenerative antioxidant activity. This review focuses on ophthalmic applications of nanoceria. Many in vivo data indicate that nanoceria protect the retina from neurodegeneration. In particular, they have been tested in animal models of age-related macular degeneration and retinitis pigmentosa and their neuroprotective properties have been shown to persist for a long time, without any collateral effects. In vitro cytotoxicity studies have shown that CeO2-NPs could be safe for lens cells and could represent a new therapy for cataract treatment, but further studies are needed. To date, different pharmaceutical formulations based on nanoceria have been created looking at future clinical ophthalmic applications, such as water-soluble nanoceria, glycol chitosan-coated ceria nanoparticles (GCCNPs), and alginate-gelatin hydrogel loaded GCCNPs. GCCNPs were also effective in preventing choroidal neovascularization in vivo. Based on the nanosize of nanoceria, corneal permeation could be achieved to allow topical treatment of nanoceria. PEGylation and encapsulation in liposomes represent the main strategies to support corneal permeation, without altering nanoceria chemical-physical properties. Based on their great antioxidant properties, safety, and nanosize, nanoceria represent a new potential therapeutic for the treatment of several eye disorders
Effetti dell'FGF-2 sull'elettroretinogramma: relazione fra fotoprotezione dei fotorecettori e sensibilità dela retina
Long-term dark rearing induces permanent reorganization in retinal circuitry
Recent data challenged the assumption that light has little effect on retina development. Here, we report evidence that dark rearing
permanently changes the synaptic input to GCs. A reduced spontaneous postsynaptic currents (SPSCs) frequency was found in retinal
GCs from rats born and raised in the dark for three months. Glutamate antagonists (CNQX and AP-5) reversibly reduced SPSCs frequency
in control and dark-reared (DR) retinae. The GABA antagonist picrotoxin (PTX) reduced SPSCs frequency in control retinas,
but increased SPSCs frequency in DR, mainly by presynaptic action on excitatory currents. In DR animals exposed to normal cyclic light
for 3 months, SPSCs frequency remained lower then in control rats and increased following PTX, suggesting that long-term dark rearing
induces permanent modifications of the retinal circuitry. Our results strongly support the idea that light stimulation plays a role in establishing
normal synaptic input to GCs
Nanoceria neuroprotective effects in the light-damaged retina: A focus on retinal function and microglia activation
The use of nanomaterials is an emerging therapeutic approach for the treatment of several pathologies. Cerium oxide nanoparticles have been studied for biomedical application, including neurodegenerative disorders, such as age-related macular degeneration in several animal models. The light damage model is characterised by oxidative stress upregulation followed by photoreceptor death and microglia activation in the outer retina. For this reason, the light damage model mimics some aspects involved in human age-related macular degeneration pathogenesis. In this review, we focus on the neuroprotective effects on retinal function and microglia activation in the light damage model, considering the administration of the nanoparticles both before and after the injury. The electrical responses of the retina and the microglia number and morphology are clearly modulated by the treatment, supporting the beneficial effects of cerium oxide nanoparticles to counteract the degeneration processes in the retina
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