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Albarracin et al. BMC Neuroscience 2013, 14:125 http://www.biomedcentral.com/1471-2202/14/125 Page 9 of 14 (A) (B) 30 25 20 15 10 5 0 (C) 40 35 30 25 20 15 10 5 0 Gene expression of Hmox1 Nontreated 670nm Treated * 5 4 3 2 1 0 * 0 3 7 10 14 C3 * 0 3 7 10 14 * Fgf-2 * 0 3 7 10 14 Days in hyperoxia (75% oxygen) Figure 10 Quantitative gene expression analyses. (A-C) Differential expression profiles of oxidative stress-inducible (A) Hmox-1, (B) proinflammatory C3 and (C) neuroprotectant Fgf-2 mRNA transcripts were measured using real time quantitative PCR. cDNAs from NT (black bar) and 670 nm-Tr (red) C57BL/6J retinas exposed to 0d, 3d, 7d, 10d 14d hyperoxia were used for quantitative analysis. The results were averaged from three independent experiments. The broken horizontal white line represents the fold change (FC) of 1 which means no change in the gene expression. The fold change of >1 represents gene upregulation while FC < 1 indicates downregulation. *Statistically significant difference (p < 0.05) between groups highlighted by the solid black horizontal line. oxidase in these retinas remained unchanged, suggesting that 670 nm light treatment maintains mitochondrial me- tabolism, leading to the attenuation of hyperoxia-induced oxidative damage. Mitochondrial dysfunction increases oxidative stress, and has been implicated in the development of several retinal degenerative conditions including AMD, diabetic retinopathy and glaucoma [42-45]. Therefore, any treat- ment strategy aimed at preventing oxidative stress may prove beneficial in slowing the progression of retinal degeneration. Several reports showed that 670 nm light treatment reduces oxidative damage, including a rat in vivo model of methanol-induced retinal toxicity [12] and animals exposed to damaging bright light [16,17]. In the latter study, the levels of expression of the oxidative damage indicators, Hmox-1 [17] and inducible nitric oxide synthase [16] were downregulated following 670 nm light treatment. Similarly, it has been reported that transcranial delivery of 670 nm light attenuates secondary oxidative damage in rat optic nerve following partial transection [46]. Moreover, findings from studies of Parkinson’s dis- ease [5,47] and Multiple Sclerosis [9] also show that treat- ment with 670 nm light mitigates oxidative stress in these experimental models. Taken together, these observations provide strong evidence that 670 nm light ameliorates oxidative damage in disorders where oxidative stress plays a key role in the progression of pathology. 670 nm light mitigates C3 expression The present study finds that exposure to hyperoxia causes a 20-fold upregulation of the complement com- ponent gene C3 in NT retinas, by 10d exposure; this Fold Change Fold Change Fold ChangePDF Image | 670 nm light mitigates oxygen-induced degeneration
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