Influence of Trace Elements on Neurodegenerative Diseases of The Eye—The Glaucoma Model

Kamińska, Agnieszka; Romano, Giovanni Luca; Ręjdak, Robert; Zweifel, Sandrine; Fiedorowicz, Michał; Rejdak, Magdalena; Bajka, Anahita; Amato, Rosario; Bucolo, Claudio; Avitabile, Teresio; Drago, Filippo; Toro, Mario Damiano

doi:10.3390/ijms22094323

Cited by 39 publications

(37 citation statements)

References 142 publications

(221 reference statements)

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“…In addition to the protective efficacy of lutein in combination with C3G, zinc and verbascoside have been reported individually as active compounds against retinal diseases. Zinc is an essential microelement that plays a main role in maintaining normal ocular function by serving as an antioxidant [ 55 ], and its supplementation is reported to slow down the progression of age-related macular degeneration [ 56 ]. Verbascoside is a glycoside present in many medicinal herbs and possesses anti-oxidative, anti-inflammatory and neuroprotective properties [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

Dietary Supplementation of Antioxidant Compounds Prevents Light-Induced Retinal Damage in a Rat Model

et al. 2021

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Light-induced retinal damage (LD) is characterized by the accumulation of reactive oxygen species leading to oxidative stress and photoreceptor cell death. The use of natural antioxidants has emerged as promising approach for the prevention of LD. Among them, lutein and cyanidin-3-glucoside (C3G) have been shown to be particularly effective due to their antioxidant and anti-inflammatory activity. However, less is known about the possible efficacy of combining them in a multicomponent mixture. In a rat model of LD, Western blot analysis, immunohistochemistry and electroretinography were used to demonstrate that lutein and C3G in combination or in a multicomponent mixture can prevent oxidative stress, inflammation, gliotic and apoptotic responses thus protecting photoreceptor cells from death with higher efficacy than each component alone. Combined efficacy on dysfunctional electroretinogram was also demonstrated by ameliorated rod and cone photoreceptor responses. These findings suggest the rationale to formulate multicomponent blends which may optimize the partnering compounds bioactivity and bioavailability.

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Section: Discussionmentioning

confidence: 99%

Dietary Supplementation of Antioxidant Compounds Prevents Light-Induced Retinal Damage in a Rat Model

et al. 2021

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“…Of them verbascoside exerts an anti-inflammatory role due to its ROS scavenging, antioxidant and iron chelating properties ( Perron and Brumaghim, 2009 ; Burgos et al, 2020 ) although its potential role in DR remains to be established. In addition to plant-derived antioxidant compounds, the activation of enzymes involved in antioxidant defenses has been related to the activity of zinc ( Kamińska et al, 2021 ). Zinc itself is not redox active but is a cofactor that exerts an indirect redox activity by regulating mitochondrial function and, therefore, the rate of ROS generation ( Marreiro et al, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Preventive Efficacy of an Antioxidant Compound on Blood Retinal Barrier Breakdown and Visual Dysfunction in Streptozotocin-Induced Diabetic Rats

et al. 2022

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In diabetic retinopathy (DR), high blood glucose drives chronic oxidative stress and inflammation that trigger alterations of the neurovascular balance finally resulting in vascular abnormalities and retinal cell death, which converge towards altered electroretinogram (ERG). In the last years, a growing body of preclinical evidence has suggested that nutrients with anti-inflammatory/antioxidant properties can be able to hamper DR progression since its very early stages. In the present study, we used a streptozotocin-induced rat model of DR, which mimics most aspects of the early stages of human DR, to test the preventive efficacy of a novel compound containing cyanidin-3-glucoside (C3G), verbascoside and zinc as nutrients with antioxidant and anti-inflammatory properties. Western blot, immunofluorescence and electroretinographic analyses demonstrated a dose-dependent inhibition of oxidative stress- and inflammation-related mechanisms, with a significant counterpart in preventing molecular mechanisms leading to DR-associated vasculopathy and its related retinal damage. Preventive efficacy of the compound on dysfunctional a- and b-waves was also demonstrated by electroretinography. The present demonstration that natural compounds, possibly as a consequence of vascular rescue following ameliorated oxidative stress and inflammation, may prevent the apoptotic cascade leading to ERG dysfunction, adds further relevance to the potential application of antioxidants as a preventive therapy to counteract DR progression.

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“…Additionally, perhaps exploitation of the newly discovered tunneling nanotubes to revive TM cells may offer some benefits in the future (Keller et al, 2017). Trace elements such a selenium, zinc, manganese and iron either alone or in combination with other drugs may also be useful in combating elevated IOP and glaucoma (Kamińska et al, 2021). Since the afore-mentioned compounds and technologies are at an early discovery stage, it is hoped that at least some of them will continue to be of clinical interest and will meet the necessary target product profile criteria to enter clinical trials in due course.…”

Section: Pharmaceutical and Cellular Therapeutics To Lower Intraocular Pressurementioning

confidence: 99%

Therapeutic Drugs and Devices for Tackling Ocular Hypertension and Glaucoma, and Need for Neuroprotection and Cytoprotective Therapies

Sharif

2021

Front. Pharmacol.

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Damage to the optic nerve and the death of associated retinal ganglion cells (RGCs) by elevated intraocular pressure (IOP), also known as glaucoma, is responsible for visual impairment and blindness in millions of people worldwide. The ocular hypertension (OHT) and the deleterious mechanical forces it exerts at the back of the eye, at the level of the optic nerve head/optic disc and lamina cribosa, is the only modifiable risk factor associated with glaucoma that can be treated. The elevated IOP occurs due to the inability of accumulated aqueous humor (AQH) to egress from the anterior chamber of the eye due to occlusion of the major outflow pathway, the trabecular meshwork (TM) and Schlemm’s canal (SC). Several different classes of pharmaceutical agents, surgical techniques and implantable devices have been developed to lower and control IOP. First-line drugs to promote AQH outflow via the uveoscleral outflow pathway include FP-receptor prostaglandin (PG) agonists (e.g., latanoprost, travoprost and tafluprost) and a novel non-PG EP2-receptor agonist (omidenepag isopropyl, Eybelis®). TM/SC outflow enhancing drugs are also effective ocular hypotensive agents (e.g., rho kinase inhibitors like ripasudil and netarsudil; and latanoprostene bunod, a conjugate of a nitric oxide donor and latanoprost). One of the most effective anterior chamber AQH microshunt devices is the Preserflo® microshunt which can lower IOP down to 10–13 mmHg. Other IOP-lowering drugs and devices on the horizon will be also discussed. Additionally, since elevated IOP is only one of many risk factors for development of glaucomatous optic neuropathy, a treatise of the role of inflammatory neurodegeneration of the optic nerve and retinal ganglion cells and appropriate neuroprotective strategies to mitigate this disease will also be reviewed and discussed.

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Influence of Trace Elements on Neurodegenerative Diseases of The Eye—The Glaucoma Model

Cited by 39 publications

References 142 publications

Dietary Supplementation of Antioxidant Compounds Prevents Light-Induced Retinal Damage in a Rat Model

Dietary Supplementation of Antioxidant Compounds Prevents Light-Induced Retinal Damage in a Rat Model

Preventive Efficacy of an Antioxidant Compound on Blood Retinal Barrier Breakdown and Visual Dysfunction in Streptozotocin-Induced Diabetic Rats

Therapeutic Drugs and Devices for Tackling Ocular Hypertension and Glaucoma, and Need for Neuroprotection and Cytoprotective Therapies

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