Neuroprotection of Rodent and Human Retinal Ganglion Cells In Vitro/Ex Vivo by the Hybrid Small Molecule SA-2

The mechanisms underlying the neuroprotective effects of the hybrid antioxidant-nitric oxide donating compound SA-2 in retinal ganglion cell (RGC) degeneration models were evaluated. The in vitro trophic factor (TF) deprivation model in primary rat RGCs and ex vivo human retinal explants were used t...

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Published in:Cells (Basel, Switzerland) Switzerland), 2022-11, Vol.11 (23), p.3741
Main Authors: Pham, Jennifer H, Johnson, Gretchen A, Rangan, Rajiv S, Amankwa, Charles E, Acharya, Suchismita, Stankowska, Dorota L
Format: Article
Language:English
Subjects:
Analysis
Animals
Apoptosis
Brain-derived neurotrophic factor
Butyl hydroperoxide
Care and treatment
Cell culture
Cell Survival
Complications and side effects
Diagnosis
Dosage and administration
Endothelin 3
Explants
Ganglion
Glaucoma
Glaucoma - drug therapy
Humans
Ischemia
Mitochondria
Neurodegeneration
Neuroprotection
Neuroprotective agents
neurotrophic factor
Nitric oxide
Optic nerve
Oxidative stress
Pathology
Rats
Reactive oxygen species
Retina
Retinal Ganglion Cells
Risk factors
Rodentia
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Summary:The mechanisms underlying the neuroprotective effects of the hybrid antioxidant-nitric oxide donating compound SA-2 in retinal ganglion cell (RGC) degeneration models were evaluated. The in vitro trophic factor (TF) deprivation model in primary rat RGCs and ex vivo human retinal explants were used to mimic glaucomatous neurodegeneration. Cell survival was assessed after treatment with vehicle or SA-2. In separate experiments, -Butyl hydroperoxide (TBHP) and endothelin-3 (ET-3) were used in ex vivo rat retinal explants and primary rat RGCs, respectively, to induce oxidative damage. Mitochondrial and intracellular reactive oxygen species (ROS) were assessed following treatments. In the TF deprivation model, SA-2 treatment produced a significant decrease in apoptotic and dead cell counts in primary RGCs and a significant increase in RGC survival in ex vivo human retinal explants. In the oxidative stress-induced models, a significant decrease in the production of ROS was observed in the SA-2-treated group compared to the vehicle-treated group. Compound SA-2 was neuroprotective against various glaucomatous insults in the rat and human RGCs by reducing apoptosis and decreasing ROS levels. Amelioration of mitochondrial and cellular oxidative stress by SA-2 may be a potential therapeutic strategy for preventing neurodegeneration in glaucomatous RGCs.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells11233741