Neurodegeneration and Neuroprotection in  Diabetic Retinopathy

Ola, Mohammad Shamsul; Nawaz, Mohd Imtiaz; Khan, Haseeb A.; Alhomida, Abdullah S.

doi:10.3390/ijms14022559

Cited by 74 publications

(58 citation statements)

References 83 publications

(98 reference statements)

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“…Pursuing neuroprotection is therefore a new therapeutic strategy in the treatment of DR [18,19]. Our results show that, following exposition to HG cell culture medium, citicoline reduced apoptosis, as already described in retinal tissue cultures [8], and reversed synapse loss.…”

Section: Resultssupporting

confidence: 78%

Neuroprotective Effects of Citicoline in in Vitro Models of Retinal Neurodegeneration

Matteucci

Varano

Gaddini

et al. 2014

IJMS

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In recent years, citicoline has been the object of remarkable interest as a possible neuroprotectant. The aim of this study was to investigate if citicoline affected cell survival in primary retinal cultures and if it exerted neuroprotective activity in conditions modeling retinal neurodegeneration. Primary retinal cultures, obtained from rat embryos, were first treated with increasing concentrations of citicoline (up to 1000 μM) and analyzed in terms of apoptosis and caspase activation and characterized by immunocytochemistry to identify neuronal and glial cells. Subsequently, excitotoxic concentration of glutamate or High Glucose-containing cell culture medium (HG) was administered as well-known conditions modeling neurodegeneration. Glutamate or HG treatments were performed in the presence or not of citicoline. Neuronal degeneration was evaluated in terms of apoptosis and loss of synapses. The results showed that citicoline did not cause any damage to the retinal neuroglial population up to 1000 μM. At the concentration of 100 μM, it was able to counteract neuronal cell damage both in glutamate- and HG-treated retinal cultures by decreasing proapoptotic effects and contrasting synapse loss. These data confirm that citicoline can efficiently exert a neuroprotective activity. In addition, the results suggest that primary retinal cultures, under conditions inducing neurodegeneration, may represent a useful system to investigate citicoline neuroprotective mechanisms.

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Section: Resultssupporting

confidence: 78%

Neuroprotective Effects of Citicoline in in Vitro Models of Retinal Neurodegeneration

Matteucci

Varano

Gaddini

et al. 2014

IJMS

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“…This includes apoptotic cell death, detected in the different layers of the retina, along with metabolic (Ola et al . ) and morphologic (Gastinger et al . ) neurodegenerative retinal changes.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Astaxanthin on Primary Retinal Cells of the GerbilPsammomys ObesusCultured in DiabeticMilieu

Baccouche

Mbarek

Dellaa

et al. 2016

Journal of Food Biochemistry

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Astaxanthin is a major marine carotenoid with powerful antioxidant and neuroprotective properties. The in vitro protective effect of astaxanthin in adult retinal cells of the type-2 diabetic model Psammomys obesus in hyperglycemic conditions was investigated. Primary retinal cells were cultured in normal (5 mM) or high concentrations of glucose (25 and 40 mM) for 5 days and treated with 1-20 μM astaxanthin for the last 48 h of culturing. Mitochondrial dehydrogenase activity and cell viability were assessed using MTT test and trypan blue exclusion dye. Retinal cells were characterized by immunohistochemistry. The results showed that mitochondrial function increased significantly (P<0.05) with 5-20 μM astaxanthin in 25-40 mM glucose. At 10 μM astaxanthin, cell viability recovered to 78.51±5.81% and 54.37±9.64% of control in 25 and 40 mM, respectively. Neurons and glial cells expression were enhanced in elevated glucose conditions. These finding suggest that astaxanthin exerted neuroprotection against high glucose induced- retinal damage. Practical Applications: The xanthophyll astaxanthin is found in many marine food sources such as shrimp. The cytoprotective and antioxidant capacity of astaxanthin in retinal disease has been pointed out and presented as a promising therapeutic strategy. The present study shows that astaxanthin can interfere with hyperglycemia-induced retinal cell death and that primary retinal culture of Psammomys obesus may represent an effective system to explore astaxanthin antioxidant mechanisms in diabetic retinopathy

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“…It was shown that the influences of ionotropic glutamatergic and GABAergic neurotransmission on the microglial process motility are indirectly mediated, via extracellular ATP which is released from neurons in response to glutamatergic signaling . ATP-induced stimulation of microglia activity may occur early in retinal disease in response to overstimulated glutamatergic transmission which is a main pathogenic factor of neuronal degeneration in many retinal disorders including ischemiaehypoxia, glaucoma, diabetic retinopathy, and inherited photoreceptor degeneration (Martin et al, 2002;Osborne et al, 2004;Delyfer et al, 2005;Ola et al, 2013).…”

Section: Purinergic Regulation Of Microglia Activitymentioning

confidence: 97%