Purchase this article with an account.
basma baccouche, Sean Donghyun Kim, Wei Wei Wang, Alistair J. Barber; Astaxanthin reduces retinal cell death and loss of neuron and glial cell markers in diabetic rats. Invest. Ophthalmol. Vis. Sci. 2017;58(8):5888.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Histological and metabolic changes are major aspects of early retinal degeneration in diabetic retinopathy. Astaxanthin (AST), a dietary carotenoid with potent antioxidant activity, has been suggested to target several health conditions. We investigated whether the administration of AST would protect the rat retina against short-term diabetes-induced damage.
Two groups of six young male Long-Evans rats were made diabetic by an injection of streptozotocin (STZ, 100 mg/kg, iv). A week after diabetes induction, a group of diabetic and non-diabetic rats were fed 1ml of astaxanthin enriched oil (AstaREAL® L10), containing 10% naturel AST, daily for eight weeks. Age-matched control and diabetic rats were given water. Nine weeks after diabetes induction, animals were sacrificed. One eye of each rat was prefixed, cryosectioned and processed for labeling against the transcription factor Brn3a, glutamine synthetase (GS) and glial fibrillary acid protein (GFAP). Cell death ELISA was performed to determine apoptosis rate on the retina of the second eye. Statistical comparisons were made by one-way ANOVA with a post hoc Tukey’s multiple comparisons test (Prism, Graphpad), with p<0.05 considered significant.
Diabetes caused a significant decrease in Brn3a expression throughout the neuroretina and was absent from retinal ganglion cell nuclei. GS and GFAP expression were also significantly reduced in STZ-diabetic rat retina compared to normal control animals. AST-treated diabetic rat retina had greater expression of Brn3a in comparison to the untreated diabetic group. In AST-treated controls and diabetic rat retina, astrocytes and Muller cells showed stronger labeling for GFAP and GS positive Muller cell processes were more intense. Cell death ELISA revealed a significant recovery in STZ-diabetic rats treated with AST when compared to untreated diabetic animals (p<0.05).
Treatment with the dietary carotenoid, AST, reduced the degeneration of retinal ganglion cells and prevented diabetes-induced retinal cell death in Long-Evans rats. AST also reduced glial cell abnormalities such as the downregulation of GFAP and GS. The results suggest that AST supplementation may provide neuroprotection in the early stages of diabetic retinopathy.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
This PDF is available to Subscribers Only