Comparison of the neuroprotective effects of brimonidine tartrate and melatonin on retinal ganglion cells

Marangoz, Deniz; Güzel, Elif; Eyuboglu, Signem; Gumusel, Asli; Seçkin, İsmail; Çiftçi, Faruk; Yılmaz, Bayram; Yalvaç, Ilgaz Saĝdiç

doi:10.1007/s10792-017-0768-z

Cited by 10 publications

(3 citation statements)

References 39 publications

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“…The efficiencies of these tracers for the retrograde labeling of RGCs have been confirmed in previous studies [ 31 , 39 – 41 ]. However, their relative advantages and disadvantages remain unclear, which may lead to their inappropriate application.…”

Section: Introductionsupporting

confidence: 73%

Did you choose appropriate tracer for retrograde tracing of retinal ganglion cells? The differences between cholera toxin subunit B and Fluorogold

et al. 2018

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Cholera toxin subunit B (CTB) and Fluorogold(FG) are two widely utilized retrograde tracers to assess the number and function of retinal ganglion cells (RGCs). However, the relative advantages and disadvantages of these tracers remain unclear, which may lead to their inappropriate application. In this study, we compared these tracers by separately injecting the tracer into the superior Colliculi (SC) in rats, one or 2 weeks later, the rats were sacrificed, and their retinas, brains, and optic nerves were collected. From the first to second week, FG displayed a greater number of labeled RGCs and a larger diffusion area in the SC than CTB; The number of CTB labeled RGCs and the diffusion area of CTB in the SC increased significantly, but there was no distinction between FG; Furthermore, CTB exhibited more labeled RGC neurites and longer neurites than FG, but no difference was evident between the same trace; The optic nerves labeled using CTB were much clearer than those labeled using FG. In conclusion, both CTB and FG can be used for the retrograde labeling of RGCs in rats at 1 or 2 weeks. FG achieves retrograde labeling of a greater number of RGCs than CTB, whereas CTB better delineates the morphology of RGCs. Furthermore, CTB seems more suitable for retrograde labeling of some small, non-image forming nuclei in the brain to which certain RGC subtypes project their axons.

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Section: Introductionsupporting

confidence: 73%

Did you choose appropriate tracer for retrograde tracing of retinal ganglion cells? The differences between cholera toxin subunit B and Fluorogold

et al. 2018

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“…Brimonidine is an α2 adrenergic agonist with extensively documented neuroprotective effects in a variety of models of retinal disease (see for instance Guo et al, 2015; Marangoz et al, 2018). In addition, in retinas of rats with STZ-induced diabetes, it has been reported to induce a significant decrease of VEGF expression and of BRB breakdown to levels similar to those observed in control rats (Kusari et al, 2010).…”

Section: Other Factorsmentioning

confidence: 99%

Relationships Between Neurodegeneration and Vascular Damage in Diabetic Retinopathy

2019

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Diabetic retinopathy (DR) is a common complication of diabetes and constitutes a major cause of vision impairment and blindness in the world. DR has long been described exclusively as a microvascular disease of the eye. However, in recent years, a growing interest has been focused on the contribution of neuroretinal degeneration to the pathogenesis of the disease, and there are observations suggesting that neuronal death in the early phases of DR may favor the development of microvascular abnormalities, followed by the full manifestation of the disease. However, the mediators that are involved in the crosslink between neurodegeneration and vascular changes have not yet been identified. According to our hypothesis, vascular endothelial growth factor (VEGF) could probably be the most important connecting link between the death of retinal neurons and the occurrence of microvascular lesions. Indeed, VEGF is known to play important neuroprotective actions; therefore, in the early phases of DR, it may be released in response to neuronal suffering, and it would act as a double-edged weapon inducing both neuroprotective and vasoactive effects. If this hypothesis is correct, then any retinal stress causing neuronal damage should be accompanied by VEGF upregulation and by vascular changes. Similarly, any compound with neuroprotective properties should also induce VEGF downregulation and amelioration of the vascular lesions. In this review, we searched for a correlation between neurodegeneration and vasculopathy in animal models of retinal diseases, examining the effects of different neuroprotective substances, ranging from nutraceuticals to antioxidants to neuropeptides and others and showing that reducing neuronal suffering also prevents overexpression of VEGF and vascular complications. Taken together, the reviewed evidence highlights the crucial role played by mediators such as VEGF in the relationship between retinal neuronal damage and vascular alterations and suggests that the use of neuroprotective substances could be an efficient strategy to prevent the onset or to retard the development of DR.

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“…There are many controversial studies on brimonidine and its effects to preserve retinal tissue. Some non-clinical findings have demonstrated that brimonidine possess retinal protective action ( Lambert et al, 2011 ; Nizari et al, 2016 ; Marangoz et al, 2018 ). However, to date, clinical trials have failed to translate into similar efficacy in humans.…”

Section: Introductionmentioning

confidence: 99%

Brimonidine is Neuroprotective in Animal Paradigm of Retinal Ganglion Cell Damage

et al. 2021

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To investigate the neuroprotective effect of brimonidine after retinal ischemia damage on mouse eye. Glaucoma is an optic neuropathy characterized by retinal ganglion cells (RGCs) death, irreversible peripheral and central visual field loss, and high intraocular pressure. Ischemia reperfusion (I/R) injury model was used in C57BL/6J mice to mimic conditions of glaucomatous neurodegeneration. Mouse eyes were treated topically with brimonidine and pattern electroretinogram were used to assess the retinal ganglion cells (RGCs) function. A wide range of inflammatory markers, as well as anti-inflammatory and neurotrophic molecules, were investigated to figure out the potential protective effects of brimonidine in mouse retina. In particular, brain-derived neurotrophic factor (BDNF), IL-6, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its death receptor DR-5, TNF-α, GFAP, Iba-1, NOS, IL-1β and IL-10 were assessed in mouse retina that underwent to I/R insult with or without brimonidine treatment. Brimonidine provided remarkable RGCs protection in our paradigm. PERG amplitude values were significantly (p < 0.05) higher in brimonidine-treated eyes in comparison to I/R retinas. Retinal BDNF mRNA levels in the I/R group dropped significantly (p < 0.05) compared to the control group (normal mice); brimonidine treatment counteracted the downregulation of retinal BDNF mRNA in I/R eyes. Retinal inflammatory markers increased significantly (p < 0.05) in the I/R group and brimonidine treatment was able to revert that. The anti-inflammatory IL-10 decreased significantly (p < 0.05) after retinal I/R insult and increased significantly (p < 0.05) in the group treated with brimonidine. In conclusion, brimonidine was effective in preventing loss of function of RGCs and in regulating inflammatory biomarkers elicited by retinal I/R injury.

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Comparison of the neuroprotective effects of brimonidine tartrate and melatonin on retinal ganglion cells

Abstract: Our study revealed that systemic administration of BRT also has an IOP reducing effect. MEL has no neuroprotective effect on RGCs; on the other hand, BRT acts as a neuroprotective agent against glaucomatous injury, when applied systemically.

Cited by 10 publications

References 39 publications

Did you choose appropriate tracer for retrograde tracing of retinal ganglion cells? The differences between cholera toxin subunit B and Fluorogold

Did you choose appropriate tracer for retrograde tracing of retinal ganglion cells? The differences between cholera toxin subunit B and Fluorogold

Relationships Between Neurodegeneration and Vascular Damage in Diabetic Retinopathy

Brimonidine is Neuroprotective in Animal Paradigm of Retinal Ganglion Cell Damage

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