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In addition to the direct effect of PBM on the gene expression and metabolism of photoreceptor cells, it is likely that other cell types in the vicinity contribute to the beneficial outcomes. Namely, research has focused on M俟ller cells which function as microgia in the retina and offer protection to photoreceptors[40-43]. Albarracin and Valter[44] demonstrated that pre-treatment with 670 nm light (prior to damaging light exposure in the rat model of light-induced retinal degeneration) resulted in amelioration of the light damage- induced changes in M俟ller cells. These included: 1) protection of the structural integrity of M俟ller cells as visualized by anti-S100茁 staining; 2) weaker stress response, as demonstrated by weaker staining with vimentin; 3) the absence of gliosis, as shown by the absence of vimentin staining in the subretinal space. The normal metabolic state was maintained, as measured by the preserved expression of glutamine synthetase in M俟ller cells, which is paramount for the clearing of the excess glutamate released by nearby photoreceptors. On the other hand, M俟ller cells are known for the production of free radicals and the secretion of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF琢) and interleukin (IL-1) in degenerating retinas. Also, early inflammatory changes in photoreceptors trigger immune responses that speed up the disease progression and M俟ller cells play a vital role in this inflammation propagation process. Interestingly, Albarracin and Valter [44] demonstrated that pre-treatment with 670 nm light in the light-induced model of retinal degeneration curbed the upregulation of TNF琢 in M俟ller cells and decreased the subsequent induction of NO synthase that produces the reactive radical NO-a major disruptor of photoreceptor metabolism[45]. In conclusion, great strides have been made towards understanding the mechanisms underlying PBM's success. Yet, ideas for the involvement of new signal transduction pathways are emerging each year and there are still many remaining pieces of the puzzle to be discovered. Role of Photobiomodulation in Retinal Health -lessons Learned from Experimental Animal Models Light-damage models of retinal degeneration and age- related macular degeneration The effects of PBM on the retina can be predicted using the known effects of PBM on other tissues and the mechanisms of retinal disease pathogenesis. In the case of AMD, Barron [46] demonstrated that cones in the aging human retina, and most prominently at the fovea, progressively accumulate mitochondrial DNA deletions and become more cytochrome C oxidase-deficient over time. Also, it is well known that inflammation, complement activation, is associated with the pathogenesis of AMD. Since both mitochondria's health and the inflammatory state are influenced by PBM, it stood to reason that FR/NIR light could treat AMD. And indeed, this was proven by Qu [47] using the rat model of light-induced AMD that features tissue damage similar to AMD pathology in humans [48]. The retinal damage in the animals was ameliorated by 670 nm LED-derived light administered 3h prior to and at 0, 24, and 48h after the light damage, for 30min each for a total of 90 J/cm2 energy density. This was demonstrated on the functional level with electro-retinogram (ERG) recordings where PBM ameliorated the decrease in the b-wave caused by the light damage. Also, there was a statistically significant decrease in cell loss as determined histopathologically measurements of the outer nuclear layer (ONL) thickness. In a study two years later, Rutar [49] demonstrated that much briefer treatments would suffice. In their mouse model of light-induced inflammatory retinal damage, pre-treatment with low-power 670 nm light for only 3min a day for 5d, delivering a total of 90 J/cm2, followed by photoreceptor- damaging bright light, resulted in reduced immune reaction with lower expression of complement genes, fewer inflammatory cells in the subretinal space, and significantly less ONL thinning compared to untreated control animals. Similar results were obtained with pre-treatment or concurrent treatment with 670 nm light in albino rats whose retinas were injured by bright light [50]. In this latter study, in addition to the animals that received 670 nm light treatment prior to the light damage, there was a group that received the treatment after the light damage. The photoreceptor function in the second group was initially reduced, as measured by ERG recordings, but recovered by one month, thus providing hope for treating patients with advanced AMD pathology. Further, the efficacy of FR/NIR phototherapy in AMD was demonstrated in a study of age-related retinal inflammation where aged mice were exposed to five 90s illuminations with 670 nm light over a 35d period, delivering a total of 18 J/cm2. The treatment reduced the macrophage numbers as well as the inflammation markers TNF and complement component 3d[51]. The results from all the studies in animal models of AMD described in this section demonstrate the potential of PBM for ameliorating and even reversing retinal damage in this all too common condition among the elderly. The efforts to translate this approach to the bedside will be described later in this review. Retinal damage in diabetes Diabetic retinopathy is a growing health concern, particularly in the developed countries where obesity keeps lowering the disease onset for type 2 diabetes. Yet, therapies aimed to preserve vision, such as laser photocoagulation, yield only a limited success and can themselves cause retinal damage. Fortunately, it might be possible to apply PBM to treat this condition, as was demonstrated in a pre-clinical study by Tang [35], using rats with streptozotocin-induced diabetes and in retinal cells exposed to harmful concentrations of glucose in their growth 陨灶贼 允 韵责澡贼澡葬造皂燥造熏 灾燥造援 9熏 晕燥援 1熏 Jan.18, 圆园16 www. IJO. cn 栽藻造押8629原愿圆圆源缘员苑圆 8629-82210956 耘皂葬蚤造押ijopress岳员远猿援糟燥皂 147PDF Image | Photobiomodulation for the treatment of retinal diseases
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