NDLI: Low-intensity far-red light inhibits early lesions that contribute to diabetic retinopathy: in vivo and in vitro.

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Low-intensity far-red light inhibits early lesions that contribute to diabetic retinopathy: in vivo and in vitro.

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Low-intensity far-red light inhibits early lesions that contribute to diabetic retinopathy: in vivo and in vitro.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tang, Johnny Talahalli, Ramaprasad Lee, Chieh Allen Kern, Timothy S. Eells, Janis T. Du, Yunpeng
Description	Country affiliation: United States Author Affiliation: Tang J ( Case Western Reserve University, Cleveland, OH 44106, USA.)
Abstract	PURPOSE: Treatment with light in the far-red to near-infrared region of the spectrum (photobiomodulation [PBM]) has beneficial effects in tissue injury. We investigated the therapeutic efficacy of 670-nm PBM in rodent and cultured cell models of diabetic retinopathy. METHODS: Studies were conducted in streptozotocin-induced diabetic rats and in cultured retinal cells. Diabetes-induced retinal abnormalities were assessed functionally, biochemically, and histologically in vivo and in vitro. RESULTS: We observed beneficial effects of PBM on the neural and vascular elements of retina. Daily 670-nm PBM treatment (6 J/cm(2)) resulted in significant inhibition in the diabetes-induced death of retinal ganglion cells, as well as a 50% improvement of the ERG amplitude (photopic b wave responses) (both P < 0.01). To explore the mechanism for these beneficial effects, we examined physiologic and molecular changes related to cell survival, oxidative stress, and inflammation. PBM did not alter cytochrome oxidase activity in the retina or in cultured retinal cells. PBM inhibited diabetes-induced superoxide production and preserved MnSOD expression in vivo. Diabetes significantly increased both leukostasis and expression of ICAM-1, and PBM essentially prevented both of these abnormalities. In cultured retinal cells, 30-mM glucose exposure increased superoxide production, inflammatory biomarker expression, and cell death. PBM inhibited all of these abnormalities. CONCLUSIONS: PBM ameliorated lesions of diabetic retinopathy in vivo and reduced oxidative stress and cell death in vitro. PBM has been documented to have minimal risk. PBM is noninvasive, inexpensive, and easy to administer. We conclude that PBM is a simple adjunct therapy to attenuate the development of diabetic retinopathy.
ISSN	01460404
e-ISSN	15525783
DOI	10.1167/iovs.12-11018
Journal	Investigative Opthalmology & Visual Science
Issue Number	5
Volume Number	54
Language	English
Publisher	Association for Research in Vision and Ophthalmology
Publisher Date	2013-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Diabetes Mellitus, Experimental Pathology Diabetic Retinopathy Radiotherapy Phototherapy Retinal Ganglion Cells Radiation Effects Animals Cell Line Metabolism Disease Models, Animal Electron Transport Complex Iv Electroretinography In Situ Nick-end Labeling In Vitro Techniques Leukostasis Neuroglia Drug Effects Nitric Oxide Oxidative Stress Physiology Photoreceptor Cells, Vertebrate Instrumentation Rats, Inbred Lew Signal Transduction Superoxides Research Support, N.i.h., Extramural Research Support, U.s. Gov't, Non-p.h.s. Discipline Ophthalmology
Content Type	Text
Resource Type	Article
Subject	Ophthalmology Sensory Systems Cellular and Molecular Neuroscience

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