Please use this identifier to cite or link to this item: http://hdl.handle.net/10316/27471
Title: Tauroursodeoxycholic acid protects retinal neural cells from cell death induced by prolonged exposure to elevated glucose
Authors: Gaspar, J. M. 
Martins, A. 
Cruz, R. 
Rodrigues, C. M. P. 
Ambrósio, A. F. 
Santiago, A. R. 
Keywords: retina; diabetes; diabetic retinopathy; TUDCA; neural apoptosis
Issue Date: 3-Dec-2013
Publisher: Elsevier
Citation: GASPAR, J. M. [et. al] - Tauroursodeoxycholic acid protects retinal neural cells from cell death induced by prolonged exposure to elevated glucose. "Neuroscience". ISSN 0306-4522. Vol. 253 (2013) p. 380-388
Serial title, monograph or event: Neuroscience
Volume: 253
Abstract: Diabetic retinopathy is one of the most frequent causes of blindness in adults in the Western countries. Although diabetic retinopathy is considered a vascular disease, several reports demonstrate that retinal neurons are also affected, leading to vision loss. Tauroursodeoxycholic acid (TUDCA), an endogenous bile acid, has proven to be neuroprotective in several models of neurodegenerative diseases, including models of retinal degeneration. Since hyperglycemia is considered to play a central role in retinal cell dysfunction and degeneration, underlying the progression of diabetic retinopathy, the purpose of this study was to investigate the neuroprotective effects of TUDCA in rat retinal neurons exposed to elevated glucose concentration. We found that TUDCA markedly decreased cell death in cultured retinal neural cells induced by exposure to elevated glucose concentration. In addition, TUDCA partially prevented the release of apoptosis-inducing factor (AIF) from the mitochondria, as well as the subsequent accumulation of AIF in the nucleus. Biomarkers of oxidative stress, such as protein carbonyl groups and reactive oxygen species production, were markedly decreased after TUDCA treatment as compared to cells exposed to elevated glucose concentration alone. In conclusion, TUDCA protected retinal neural cell cultures from cell death induced by elevated glucose concentration, decreasing mito-nuclear translocation of AIF. The antioxidant properties of TUDCA might explain its cytoprotection. These findings may have relevance in the treatment of diabetic retinopathy patients.
URI: http://hdl.handle.net/10316/27471
ISSN: 0306-4522
DOI: 10.1016/j.neuroscience.2013.08.053
Rights: openAccess
Appears in Collections:I&D CNC - Artigos em Revistas Internacionais
FMUC Medicina - Artigos em Revistas Internacionais
I&D IBILI - Artigos em Revistas Internacionais

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